Chlamydial Respiratory Infection during Allergen Sensitization Drives Neutrophilic Allergic Airways Disease

Horvat, Jay C.; Starkey, Malcolm R.; Kim, Richard; Beagley, Kenneth W.; Preston, Julie A.; Gibson, Peter G.; Foster, Paul S.; Hansbro, Philip M.

doi:10.4049/jimmunol.0902287

Cited by 85 publications

(112 citation statements)

References 68 publications

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“…injection of OVA (day 0, 50 mg; Sigma, St Louis, MO, USA) in Rehydrogel (1 mg; Reheis, Berkeley Heights, NJ, USA) and sterile saline (200 mL), and subsequently challenged (progression of AAD) by intranasal delivery of OVA (day 12-15, 10 mg in 50 mL sterile saline; figs 1-3) [8,16,17]. Mice were sacrificed and AAD was assessed 1 day later (day 16).…”

Section: Allergic Sensitisation and Challengementioning

confidence: 99%

Streptococcus pneumoniaeinfection suppresses allergic airways disease by inducing regulatory T-cells

Preston¹,

Thorburn²,

Starkey³

et al. 2010

Eur Respir J

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An inverse association exists between some bacterial infections and the prevalence of asthma. We investigated whether Streptococcus pneumoniae infection protects against asthma using mouse models of ovalbumin (OVA)-induced allergic airway disease (AAD).Mice were intratracheally infected or treated with killed S. pneumoniae before, during or after OVA sensitisation and subsequent challenge. The effects of S. pneumoniae on AAD were assessed.Infection or treatment with killed S. pneumoniae suppressed hallmark features of AAD, including antigen-specific T-helper cell (Th) type 2 cytokine and antibody responses, peripheral and pulmonary eosinophil accumulation, goblet cell hyperplasia, and airway hyperresponsiveness. The effect of infection on the development of specific features of AAD depended on the timing of infection relative to allergic sensitisation and challenge. Infection induced significant increases in regulatory T-cell (Treg) numbers in lymph nodes, which correlated with the degree of suppression of AAD. Tregs reduced T-cell proliferation and Th2 cytokine release. The suppressive effects of infection were reversed by anti-CD25 treatment.Respiratory infection or treatment with S. pneumoniae attenuates allergic immune responses and suppresses AAD. These effects may be mediated by S. pneumoniae-induced Tregs. This identifies the potential for the development of therapeutic agents for asthma from S. pneumoniae.

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Section: Allergic Sensitisation and Challengementioning

confidence: 99%

Streptococcus pneumoniaeinfection suppresses allergic airways disease by inducing regulatory T-cells

Preston¹,

Thorburn²,

Starkey³

et al. 2010

Eur Respir J

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“…In addition, some researchers observed that C. pneumoniae can induce asthma (Horvat et al, 2010a(Horvat et al, , 2010bStarkey et al, 2012). It has been reported (Jahnsen et al, 2006;Ahmed et al, 2007;Goleva et al, 2008) that NRI-induced asthma may be associated with neural regulatory mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Distribution of pathogens causing nosocomial infection in patients with bronchial asthma

Mao¹,

Cui²

2015

Genet. Mol. Res.

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ABSTRACT.This study aimed to analyze nosocomial respiratory infection (NRI) in patients with bronchial asthma. Among the clinical data of 575 asthmatic patients that was collected and analyzed, 52 were diagnosed with NRI. The most common gram-positive bacterial species was Streptococcus pneumoniae, which was detected in 8 patients, whereas the predominant Gram-negative bacteria included Haemophilus influenzae (11 patients), Moraxella catarrhalis (8 patients), and Escherichia coli (7 patients). The simultaneous detection of all strains was predominant in patients older than 65 years of age, whereas the detection rates of S. pneumoniae, H. influenzae, E. coli, and M. catarrhalis were predominant in patients younger than 65 years old. The differences in the detection rates were not significant between the male and female groups. From this study, we can conclude that S. pneumoniae, H. influenzae, E. coli, and M. catarrhalis are common NRI-causing pathogens, and bacterial infection is the main risk factor for NRI in asthmatic patients.

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“…Bronchoalveolar lavage (BAL) was performed as previously described, and differential leukocyte counts were determined from a total of 250 cells (15,16).…”

Section: Assessment Of Airway Inflammationmentioning

confidence: 99%

“…Airway hyperresponsiveness AHR was assessed as described previously (13)(14)(15). Briefly, anesthetized and tracheotomized mice were cannulated and connected to inline aerosol and ventilator apparatus.…”

Section: T Cell Cytokine Releasementioning

confidence: 99%

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Pneumococcal Components Induce Regulatory T Cells That Attenuate the Development of Allergic Airways Disease by Deviating and Suppressing the Immune Response to Allergen

Thorburn

Brown

Nair

et al. 2013

The Journal of Immunology

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The induction of regulatory T cells (Tregs) to suppress aberrant inflammation and immunity has potential as a therapeutic strategy for asthma. Recently, we identified key immunoregulatory components of Streptococcus pneumoniae, type 3 polysaccharide and pneumolysoid (T+P), which suppress allergic airways disease (AAD) in mouse models of asthma. To elucidate the mechanisms of suppression, we have now performed a thorough examination of the role of Tregs. BALB/c mice were sensitized to OVA (day 0) i.p. and challenged intranasal (12–15 d later) to induce AAD. T+P was administered intratracheally at the time of sensitization in three doses (0, 12, and 24 h). T+P treatment induced an early (36 h–4 d) expansion of Tregs in the mediastinal lymph nodes, and later (12–16 d) increases in these cells in the lungs, compared with untreated allergic controls. Anti-CD25 treatment showed that Treg-priming events involving CD25, CCR7, IL-2, and TGF-β were required for the suppression of AAD. During AAD, T+P-induced Tregs in the lungs displayed a highly suppressive phenotype and had an increased functional capacity. T+P also blocked the induction of IL-6 to prevent the Th17 response, attenuated the expression of the costimulatory molecule CD86 on myeloid dendritic cells (DCs), and reduced the number of DCs carrying OVA in the lung and mediastinal lymph nodes. Therefore, bacterial components (T+P) drive the differentiation of highly suppressive Tregs, which suppress the Th2 response, prevent the Th17 response and disable the DC response resulting in the effective suppression of AAD.

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Chlamydial Respiratory Infection during Allergen Sensitization Drives Neutrophilic Allergic Airways Disease

Abstract: Material

Cited by 85 publications

References 68 publications

Streptococcus pneumoniaeinfection suppresses allergic airways disease by inducing regulatory T-cells

Streptococcus pneumoniaeinfection suppresses allergic airways disease by inducing regulatory T-cells

Distribution of pathogens causing nosocomial infection in patients with bronchial asthma

Pneumococcal Components Induce Regulatory T Cells That Attenuate the Development of Allergic Airways Disease by Deviating and Suppressing the Immune Response to Allergen

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