Cemiplimab jest przeciwciałem monoklonalnym przeciw PD-1, które w Europie posiada rejestrację w monoterapii u chorych na NDRP z ekspresją PD-L1 ≥ 50% oraz w połączeniu z chemioterapią w grupie z ekspresją PD-L1 ≥ 1%. W Polsce zastosowanie cemiplimabu jest możliwe w wymienionych wskazaniach w ramach programu lekowego B6. W badaniu klinicznym EMPOWER-Lung 1 wykazano znamienną poprawę czasu całkowitego przeżycia -OS (HR – 0.57) i przeżycia wolnego od progresji-PFS (HR - 0.51) na korzyść cemiplimabu przy mniejszym ryzyku działań niepożądanych w porównaniu do samej chemioterapii. Zastosowanie cemiplimabu w połączeniu z chemioterapią znamiennie poprawia OS (HR - 0.65) i PFS, (HR - 0.55) oraz zwiększa odsetek odpowiedzi obiektywnych. Skuteczność cemiplimabu w połączeniu z chemioterapią jest ograniczona do grupy chorych z ekspresją PDL1 >1% i jest obserwowana niezależnie od typu histologicznego NDRP. Profil toksyczności cemiplimabu jest charakterystyczny dla grupy przeciwciał anty PD1 i anty PD-L1. Badania oceniające jakość życia chorych wskazują, że leczenie cemiplimabem wiąże się z mniejszym ryzykiem pogorszenia jakości życia w porównaniu do chemioterapii. Cemiplimab stosowany w monoterapii lub w połączeniu z chemioterapią jest jedną z aktualnie dostępnych w Polsce opcji terapeutycznych i znajduje

Patients with unresectable stage III non–small cell lung cancer (NSCLC) who experience disease progression after chemoradiotherapy and consolidation durvalumab represent a growing population with poor outcomes and no established standard of care. Despite the survival benefit demonstrated in the PACIFIC trial, early disease progression remains frequent, and optimal management in this setting is not well defined. In this multicenter retrospective real-world study, we analyzed patterns of disease progression and post-progression treatment strategies in 60 patients treated with chemoradiotherapy followed by durvalumab, with a particular focus on time to next systemic treatment (TNST) as a clinically relevant endpoint reflecting treatment sequencing. Disease progression was heterogeneous in both timing and location. Locoregional progression was associated with a longer time to subsequent treatment compared with distant or combined progression. Importantly, the use of radical local salvage therapy was associated with a clinically meaningful delay in the initiation of subsequent systemic treatment, with median TNST of 29.1 months compared with 12.6 months in patients receiving palliative or no local intervention. TNST showed strong associations with other key clinical outcomes. These findings support its role as a pragmatic real-world endpoint capturing treatment trajectories after consolidation immunotherapy. These findings suggest that carefully selected patients with limited post-durvalumab progression may benefit from radical local salvage therapy, which may delay the need for subsequent systemic treatment in a setting with no established standard of care. Our results support the integration of local ablative strategies into multidisciplinary decision-making and highlight TNST as a clinically meaningful endpoint in this context.

The current standard of care (SoC) for patients with extensive-disease small-cell lung cancer (ED-SCLC) is chemo-immunotherapy. The efficacy of radiotherapy (RT) for chest consolidation has been established for patients with ED-SCLC who have responded to chemotherapy. There is a lack of data on incorporating RT as chest consolidation and metastasis-directed therapy for ED-SCLC. The RISE (Radiotherapy for Extensive-Stage Small-Cell Lung Cancer) study aims to evaluate the effectiveness of different RT strategies for residual lesions for patients with ED-SCLC who receive chemo-immunotherapy. A total of 165 patients with ED-SCLC will be recruited, with 55 patients assigned to each of the three study arms. Patients with stabilization or partial regression, according to the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, during chemo-immunotherapy will be included. • Arm I will serve as the control group, comprising patients who continue SoC of programmed death-ligand 1 (PD-L1)/programmed death-1 (PD-1) immunotherapy (durvalumab or atezolizumab) following platinum-based chemo-immunotherapy. • Arm II will receive the SoC with consolidative RT to the chest area and potentially, according to palliative indications to metastatic lesions, delivered in 30 Gy in 3-Gy fractions. • Arm III will receive SoC with RT of 45 Gy in 3-Gy fractions to the chest area and stereotactic body radiotherapy (SBRT) with 24 Gy in 8-Gy fractions to the metastatic lesions. Blood samples for circulating tumor DNA (ctDNA) will be collected before RT, during each week of treatment, and at the time of disease progression. The primary endpoint is progression-free survival (PFS) based on RECIST 1.1 or patient death. 1. Secondary endpoints are OS, treatment toxicity (frequency of G3 toxicity according to CTCAE v.5.0), area of progression (primary tumor localization/new lesions), Overall response rate (ORR), and the response rate in non-irradiated lesions. The study population of patients with ED-SCLC has a poor prognosis. Dose-escalated chest RT and SBRT (for up to 10 metastases) administered with modern techniques offer the possibility to improve OS and PFS. Clinicaltrials.gov NCT06529081 (Registered 26th Jul 2024).

Cemiplimab is a monoclonal antibody against PD-1, which has European approval for monotherapy in patients with NSCLC with PD-L1 expression > 50% and in combination with chemotherapy in a group with PDL1 expression > 1%. In Poland, the use of cemiplimab is possible in these indications according to the criteria of the drug program B.6. The EMPOWER-Lung 1 trial showed significant improvement in OS (HR = 0.57) and PFS (HR = 0.51) in favor of cemiplimab with a lower risk of adverse events compared to chemotherapy alone. The use of cemiplimab in combination with chemotherapy significantly improves OS (HR = 0.65) and PFS (HR = 0.55) and increas-es objective response rates. The efficacy of cemiplimab in combination with chemotherapy is limited to the group of patients with PD-L1 expression > 1% and is observed regardless of the histological type of NSCLC. The toxicity profile of cemiplimab is characteristic of the anti-PD-1 and anti-PD-L1 antibody groups. Studies evaluating patients' quality of life indicate that cemiplimab treatment is associated with a lower risk of worsening quality of life compared to chemotherapy. When used as monotherapy or in combination with chemotherapy, cemiplimab is one of the currently available therapeutic options and has reasonable use in relevant patient populations.

Background/Objectives: Influenza is a viral infection affecting up to 20% of the general population annually. Solid organ transplant recipients have a higher morbidity and mortality risk, as well as a greater likelihood of severe disease complications. Vaccination against the influenza virus is a safe and recommended prophylaxis; however, immunosuppression and high comorbidity burdens impair the immune response. We assessed the efficacy, safety, and humoral response to influenza vaccine in a population of kidney transplant recipients (KTx). Methods: Adult KTx recipients at least 6 months post-KTx were divided into vaccinated (vKTx) and non-vaccinated (nvKTx) groups based on consent for vaccination. The vKTx group received one dose of quadrivalent split virion inactivated vaccine (Vaxigrip Tetra Sanofi Pasteur). Subjective symptoms and side effects were recorded in paper journals. Antibody levels were assessed with ELISA prior to and 3 months following vaccination. Serum creatinine and proteinuria were assessed prior to vaccination as well as 3 and 6 months after. Results: Of 450 recruited KTx recipients, 91 in the vKTx group and 36 in the nvKTx group of comparable age, KTx vintage, and graft function were included in the study. Graft function and proteinuria remained stable in both groups. The vKTx group experienced no severe adverse events. The most common complaints were general malaise (20.5%) and injection site pain (10.3%). Overall infection rates were comparable, yet the vKTx group experienced significantly fewer serious infections (11.4% vs. 32.3%, p = 0.01); the vKTx group showed a greater increase of Influenza A IgM (p = 0.05) and Influenza B IgG (p = 0.01) compared with the nvKTx group. Conclusions: Influenza vaccination prevents severe infections in KTx recipients, with good serological response and no impact on graft function or severe adverse events.

Circulating free DNA (cfDNA) is genetic material released from various cells into bodily fluids. Among its fractions, circulating tumor DNA (ctDNA) originates from tumor cells and reflects their genetic material, including mutations and epigenetic changes. Methods commonly employed for detecting ctDNA in blood include next-generation sequencing (NGS) and various types of PCR. The presence of ctDNA can be utilized in liquid biopsies for many diagnostic purposes related to various cancers. It is a minimally invasive method of sampling molecular compounds from tumor cells. In this paper, we focus on current knowledge regarding the liquid biopsy of blood ctDNA in the context of lung cancer, one of the leading causes of cancer-related mortality. Currently, as a clinically approved method, liquid biopsy serves as a complementary technique in NSCLC diagnostic and genetic profiling. Other applications of liquid biopsy that are still being investigated include the detection of minimal residual disease (MRD) after curative treatment and response monitoring to systemic treatment. This review discusses current and future potential directions for the development and implementation of ctDNA for patients with NSCLC.

Studies have shown that eosinophilic COPD (eCOPD) is a distinct phenotype of the disease. It is well established that innate lymphoid cells are involved in the development of eosinophilic inflammation. Interleukin(IL)-25, thymic stromal lymphopoietin (TSLP) and IL-33 are a group of cytokines produced by epithelium in response to danger signals, e.g., cigarette smoke, and potent activators of ILC2s. In the present study, we examined circulating and sputum ILC2 numbers and expression of intracellular IL-5 as well as receptors for TSLP, IL-33 and IL-25 by ILC2s in non-atopic COPD patients with and without (neCOPD) airway eosinophilic inflammation and healthy smokers. In addition, we examined the association between ILC2s and clinical indicators of COPD burden (i.e., symptom intensity and risk of exacerbations). ILC2s were enumerated in peripheral blood and induced sputum by means of flow cytometry. We noted significantly greater numbers of airway IL-5+ILC2s and TSLPR+ILC2s in eCOPD compared with neCOPD (p < 0.05 and p < 0.01, respectively) and HSs (p < 0.001 for both). In addition, we showed that IL-5+ILC2s, IL-17RB+ILC2s and ST2+ILC2s are significantly increased in the sputum of eCOPD patients compared with HSs. In all COPD patients, sputum ILC2s positively correlated with sputum eosinophil percentage (r = 0.48, p = 0.002). We did not find any significant correlations between sputum ILC2s and dyspnea intensity as measured by the modified Medical Research Council scale (mMRC) and symptom intensity measured by the COPD Assessment Test (CAT). These results suggest the involvement of epithelial alarmin-activated ILC2s in the pathobiology of eosinophilic COPD.

INTRODUCTION The procedure of lung parenchyma resection may result in impairment of physical capacity and quality of life. In patients with operable non-small cell lung cancer (NSCLC), lobectomy is an elective procedure. Chronic obstructive pulmonary disease (COPD) is a common coexisting condition in patients with NSCLC. Effectiveness of post-operative pulmonary rehabilitation (PR) in patients who underwent lobectomy due to NSCLC and suffering from COPD as compared to individuals without COPD has not been determined yet. The aim of the study was to compare effectiveness of post-operative PR in patients with COPD after lobectomy due to NSCLC (COPD[+] L [+]) with individuals with COPD without lung parenchyma resection (COPD(+) L(-)) and those who underwent lobectomy due to NSCLC and not suffering from COPD (COPD[-] L[+]). MATERIAL AND METHODS Thirty-seven patients with non-small cell lung cancer (21 patients with and 16 patients without COPD) who underwent lobectomy and 29 subjects with COPD referred to the Lung Diseases Treatment and Rehabilitation Centre in Lodz in 2018-2019 were included in this retrospective analysis. The patients participated in a 3-week inpatient pulmonary rehabilitation (PR) program which included breathing exercises, physical workout, relaxation exercises, education, psychological support and nutrition consulting. The evaluation included lung function measurements, six-minute walking test (6MWT) and the St. George's Respiratory Questionnaire (SGRQ) score. The results obtained before the rehabilitation were compared to those achieved after the 3-week PR program and compared between the study groups. RESULTS A significant increase in the distance covered during 6MWT was observed in all the three groups studied: COPD(+) L(+) (Δ = 62.52 ± 14.58 m); COPD(-) L(+) (Δ = 73.67 ± 11.58 m); and COPD(+) L(-) (Δ = 59.93 ± 10.02 m) (p < 0.001 for all). Similarly, a statistically and clinically significant improvement in the total SGRQ score was recorded: COPD(+) L(+) ∆ = -12.05 ± 3.96 points; p < 0.05 and COPD(-) L(+) ∆ = -12.30 ± 4.85 points; p < 0.01 and COPD(+) (L-) ∆= -14.07 ± 3.36 points (p < 0.001). No significant differences in the outcome improvement between the study groups were identified. CONCLUSIONS The results of the study show that COPD(+) L(+) patients gained benefits from post-operative PR comparable to COPD(+) L(-) and COPD(-) L(+) subjects by improving their physical capacity and quality of life.

3. Huang K, Yang T, Xu J, et al. Prevalence, risk factors, and management of asthma in China: a national cross-sectional study. Lancet. 2019;394(10196):407-418. 4. Tay TR, Hew M. Comorbid, "treatable traits" in difficult asthma: Current evidence and clinical evaluation. Allergy. 2018;73(7):1369-1382. 5. Ciprandi G, Schiavetti I, Rindone E, et al. The impact of anxiety and depression on outpatients with asthma. Ann Allergy Asthma Immunol. 2015;115(5):408-414. 6. Oga T, Nishimura K, Tsukino M, et al. Analysis of longitudinal changes in the psychological status of patients with asthma. Respir Med. 2007;101(10):2133-2138. 7. Shen H, Hua W, Wang P, et al. A new phenotype of asthma: chest tightness as the sole presenting manifestation. Ann Allergy Asthma Immunol. 2013;111(3):226-227. 8. Hakola R, Kauppi P, Leino T, et al. Persistent asthma, comorbid conditions and the risk of work disability: a prospective cohort study. Allergy. 2011;66(12):1598-1603. 9. Mancuso CA, Wenderoth S, Westermann H, et al. Patient-reported and physician-reported depressive conditions in relation to asthma severity and control. Chest. 2008;133(5):1142-1148.

TYPE: Abstract Publication TOPIC: Obstructive Lung Diseases PURPOSE: Recent data show that fibrocytes may play a role in COPD pathogenesis and may be activated by epithelium-derived substances. The aim of this study was to assess epithelial alarmin expression (IL-17RB, ST2 and TSLPR) on circulating fibrocytes in eosinophilic vs non-eosinophilic COPD. METHODS: 22 (12 eosinophilic) COPD patients were recruited. All patients were non-atopic based on negative results of skin prick testing. None of the patients were on inhaled corticosteroid treatment. eCOPD was defined as sputum eosinophilia >3%. Alarmin receptor expression on circulating fibrocytes was assessed by means of flowcytometry. Fibrocytes were defined as CD45+CD15−Lin−CXCR4+Col-1+ cells. RESULTS: There was no difference in the number of circulating fibrocytes between eCOPD and neCOPD. However, there was a higher number of circulating TSLPR+fibrocytes in eCOPD vs neCOPD (60.66±18.12 vs 14.69±4.62 cells/1 mln of PBMC, respectively; p=0.0258). There were no significant differences in the number of circulating ST2+ and IL-17RB+fibrocytes between the study groups. CONCLUSIONS: Increased number of TSLPR+fibrocytes may indicate involvement of TSLP-activated fibrocytes in the pathogenesic of eosinophilic COPD. Funding: National Science Centre, grant no: 2017/26/NZ5/00468 CLINICAL IMPLICATIONS: TSLP and fibrocytes may be potential targets in the treatment of eosinophilic COPD. DISCLOSURE: No significant relationships. KEYWORDS: alarmins, fibrocytes, COPD

Objectives: To assess the safety and clinical efficacy after 3 months treatment of COPD by autologous stem cells from adipose tissue.Subjects: 9 patients COPD over 40 years old with FEV1 <60% and having at least two exacerbations or a hospitalization in 12 months ago were received autologous stem cells from adipose tissue from 8/2018 to 3/2019.Methods: clinical trial.Result: 9 patients did not experience any adverse events.An improvement of dyspnoea and quality of life in 9 patients with mean values before and after 3 months treatment of the CAT index was 23.4 AE 7.84 and 18, 6 AE 9,86; SGRQ is 51.6 AE 17.05 and 48 AE 15.6, BODE is 8.5 AE 1.66 and 7.3 AE 1.22.8/9 patients increased their walking distance by 6 minutes with an average value of 341.7 AE 93.74 (meters) to 426.6 AE 112.52 (meters).No changes in blood gas index and respiratory function at 3 months after stem cell treatment.Conclusion: Initial treatment for COPD with autologous stem cells from adipose tissue is safe and improves dyspnoea, quality of life for patients.

INTRODUCTION:Interleukin (IL)-25, IL-33 and thymic stromal lymphopoietin (TSLP) are epithelial alarmins involved in innate immune responses and have been shown to play an important role in chronic lung diseases. No data are available regarding their levels in exhaled breath condensate (EBC) in idiopathic pulmonary fibrosis (IPF).OBJECTIVES:To examine IL-25, IL-33 and TSLP levels in the EBC obtained from patients with IPF and compare them to those in healthy controls, patients with asthma and chronic obstructive pulmonary disease (COPD).METHODS:Twenty-three patients with asthma, 25 patients with COPD, 15 patients with IPF and 16 healthy controls were studied. Concentrations of alarmins in the EBC were evaluated by means of ELISA.RESULTS:IL-25 EBC levels were numerically lowest in IPF (25.33 ± 8.84 pg/ml). However, they did not differ significantly from healthy subjects (43.18 ± 5.53 pg/ml), but were significantly lower compared to asthma (72.07 ± 6.03 pg/ml; P < .001). IL-33 EBC levels were significantly increased in IPF (3.41 ± 0.55 pg/ml) compared to healthy controls (1.20 ± 0.60 pg/ml; P < .01) but did not differ from asthma (3.68 pg/ml) and COPD levels (2.47 ± 0.34 pg/ml). There were significant correlations between IL-33 EBC levels and lung diffusion capacity of carbon monoxide (DLco ) absolute (r = .63; P < .05) and % of predicted values (r = .67; P < .01) as well as with time since diagnosis (r = -.59; P < .05) in IPF subjects. TSLP was undetectable in examined samples.CONCLUSION:IL-25 and IL-33 are detectable in the EBC obtained from IPF subjects. Increased levels of IL-33 compared to healthy controls indicate its possible role in the pathobiology of IPF.

Przewlekła obturacyjna choroba płuc (POChP) była tradycyjnie uważana za jednostkę, w której dominuje zapalenie neutrofilowe oskrzeli. Wyniki badań z początku lat 90. ubiegłego wieku wykazały, że również eozynofile napływają do dolnych dróg oddechowych chorych na POChP, a ich zwiększona liczba jest obserwowana zarówno w trakcie zaostrzeń, jak i w stabilnym okresie choroby. Fenotyp eozynofilowego POChP odznacza się kilkoma unikatowymi cechami, tj. specyficznym charakterem zapalenia dróg oddechowych i przebiegiem klinicznym oraz podatnością na terapię glikortykosteroidami. W niniejszym artykule zaprezentowano przegląd aktualnych badań dotyczących charakterystyki klinicznej pacjentów z eozynofilowym fenotypem POChP, jak również rolę eozynofilów jako biomarkera użytecznego w podejmowaniu decyzji terapeutycznych w POChP.

Background: Previous murine models have demonstrated interleukin (IL)-33 to be an important mediator of type-2 inflammation and to promote airway hyperresponsiveness in allergic asthma. A number of inflammatory cells produce IL-33 and eosinophils express ST2 mRNA. The relationship between IL-33 and eosinophils in allergic asthma, however, remains unclear. Objective: The aim of this work was to evaluate in vitro the effect of allergen inhalation on IL-33 levels and expression of its receptor (ST2L) on eosinophils in allergic asthmatics, and the effect of IL-33 stimulation on eosinophil activity. Methods: Plasma and sputum IL-33, soluble ST2 (sST2) levels, and ST2L expression on eosinophils were measured in 10 healthy controls and 10 allergic asthmatics. Asthmatics underwent allergen and diluent inhalation challenges. Blood and sputum samples were collected to measure IL-33, sST2, and ST2L eosinophil expression before and 24 h after allergen inhalation. Purified blood eosinophils from allergic asthmatics were incubated overnight with IL-33 to assess ST2 and intracellular IL-5 expression. Results: Baseline levels of IL-33 in sputum and sST2 in plasma and sputum were similar in allergic asthmatics compared to healthy controls. In addition, there was no difference in blood or sputum eosinophil ST2L expression in healthy controls versus allergic asthmatics. Eosinophil ST2L expression was significantly increased 24 h postallergen inhalation in allergic asthmatics. In vitro stimulation of human eosinophils with IL-33 and LPS significantly increased eosinophil ST2L expression and IL-33 stimulation increased intracellular IL-5 expression, which was attenuated by treatment with sST2 and ST2 blockade. Conclusion and Clinical Relevance: In mild asthmatics, there was a significant upregulation of ST2 surface expression on eosinophils from blood and sputum following allergen inhalation challenge. In vitro, IL-33 stimulation of eosinophils increases both ST2 membrane expression and IL-5 production. These results support a role for IL-33 in causing allergen-induced eosinophilia. Blockade of IL-33 and ST2 signaling may present a novel therapeutic avenue for asthma treatment.

Background Despite the absence of endogenous chitin in humans, chitinases are present in the serum of healthy subjects and their levels are increased in a variety of chronic inflammatory conditions. It has been shown that chitotriosidase and structurally related chitinase-like protein-YKL-40 contribute to the pathogenesis of COPD. However, details regarding the relation of their systemic and local airways levels remain unknown. Objectives To examine peripheral blood and sputum chitotriosidase and YKL-40 expression in smokers and patients with COPD. Methods Forty patients with COPD, 20 healthy smokers and 10 healthy never-smokers were studied. Serum and induced sputum chitotriosidase protein and activity levels, YKL-40 concentrations, and their gene expression in sputum cells and peripheral blood mononuclear cells (PBMC) were evaluated. Results Both chitotriosidase protein levels and activity were higher in sputum obtained from COPD subjects compared to healthy never-smokers (P<0.05 and P<0.01, respectively). A similar pattern was observed for PBMC chitotriosidase mRNA expression (P<0.001). YKL-40 serum concentrations were elevated in healthy smokers and COPD subjects compared to healthy never-smokers (P<0.001 and P<0.01, respectively). In sputum, YKL-40 levels were increased in COPD compared to healthy never-smokers (P<0.01). PBMC YKL-40 mRNA expression was increased in COPD and healthy smokers compared to healthy never-smokers (P<0.0001). No associations were found between chitotriosidase or YKL-40 peripheral blood levels and sputum levels. Conclusions Our results demonstrate that chitotriosidase and YKL-40 are overexpressed in peripheral blood and airways in both healthy smokers and COPD subjects which may indicate smoking-related activation of macrophages, neutrophils, and epithelial cells.

Interleukin(IL)-33 is an epithelial alarmin important for eosinophil maturation, activation and survival. The aim of this study was to examine the association between IL-33, its receptor expression and airway eosinophilic inflammation in non-atopic COPD.

SummaryBackgroundHaemopoietic progenitor cells (HPC) migrate to sites of allergic inflammation where, upon stimulation with epithelial cytokines, they produce Th2 cytokines and differentiate into mature eosinophils and basophils. They also express Toll‐like receptors (TLR) involved in antimicrobial responses.ObjectiveThe objective of this study was to compare TLR expression on peripheral blood HPC and TLR‐induced responses, in particular changes in epithelial cytokine receptors, in healthy and asthmatic subjects at baseline and following allergen challenge.MethodsTen healthy and 11 allergic asthmatic subjects were studied. HPC‐enriched cell populations were stimulated with TLR‐2, TLR‐4 or TLR‐9 ligands. TLR expression by circulating HPC and interleukin (IL)‐25 (IL‐17RB), IL‐33 (ST2) and thymic stromal lymphopoietin receptor (TSLPR) expression after TLR ligation were examined by flow cytometry at baseline and, in asthmatics, following allergen challenge. The effects of dexamethasone (Dex) on TLR‐induced responses were also assessed.ResultsAsthmatics had significantly lower circulating HPC expressing TLR‐2 and TLR‐9 with a similar trend for TLR‐4. TLR‐4 stimulation of HPC yielded higher numbers of TSLPR+ cells in asthmatics compared with healthy subjects. A similar trend was seen for TLR‐9 ligation, an effect further augmented by allergen inhalation. Allergen challenge also enhanced TLR‐induced ST2 expression on HPC. Treatment with Dex in vitro increased TLR‐4‐induced TSLPR expression but had no effect on other epithelial cytokine receptors.Conclusions and Clinical RelevanceThese data demonstrate an interaction between allergen and TLR ligand exposure in asthmatics. Allergen inhalation augments the TLR‐induced inflammatory response by HPC, possibly leading to increased “in situ haemopoiesis” through up‐regulation of TSLPR. These findings show that HPC may be a part of the pro‐inflammatory cascade in pathogen‐induced asthma exacerbation through their increased responsiveness to TLR stimulation.