Immune response to Streptococcus pneumoniae in asthma patients: comparison between stable situation and exacerbation

Abstract

SummaryIn Argentina, more than 3 million people suffer from asthma, with numbers rising. When asthma patients acquire viral infections which, in turn, trigger the asthmatic response, they may develop subsequent bacterial infections, mainly by Streptococcus (S.) pneumoniae. This encapsulated Gram + bacterium has been considered historically a T cell-independent antigen. Nevertheless, several papers describe the role of T cells in the immune response to S. pneumoniae. We evaluated the response to S. pneumoniae and compared it to the response to Mycobacterium (M.) tuberculosis, a different type of bacterium that requires a T helper type 1 (Th1) response, in cells from atopic asthmatic children, to compare parameters for the same individual under exacerbation and in a stable situation whenever possible. We studied asthma patients and a control group of age-matched children, evaluating cell populations, activation markers and cytokine production by flow cytometry, and cytokine concentration in serum and cell culture supernatants by enzymelinked immunosorbent assay (ELISA). No differences were observed in gd T cells for the same patient in either situation, and a tendency to lower percentages of CD4 + CD25 hi T cells was observed under stability. A significantly lower production of tumour necrosis factor (TNF)-a and a significantly higher production of interleukin (IL)-5 was observed in asthma patients compared to healthy individuals, but no differences could be observed for IL-4, IL-13 or IL-10. A greater early activation response against M. tuberculosis, compared to S. pneumoniae, was observed in the asthmatic patients' cells. This may contribute to explaining why these patients frequently acquire infections caused by the latter bacterium and not the former.

Microbiota associations with inflammatory pathways in asthma

“…The expression of lymphocyte activation marker CD69 was increased by Streptococcus pneumoniae antigen. 29 CD69 plays an important role in the pathogenesis of allergen-induced eosinophilic airway inflammation and hyperresponsiveness 30 and inhibits Th17 cell differentiation through activating JAK3-STAT5 pathways. 31 Th17 cells, via IL-17A and IL-17F, promote neutrophil recruitment and have been invoked as a noneosinophilic/non-type 2 pathway in asthma.…”

“…Streptococcus pneumoniae has been widely believed to be associated with asthma via immune modulation. The expression of lymphocyte activation marker CD69 was increased by Streptococcus pneumoniae antigen 29 . CD69 plays an important role in the pathogenesis of allergen‐induced eosinophilic airway inflammation and hyperresponsiveness 30 and inhibits Th17 cell differentiation through activating JAK3‐STAT5 pathways 31 .…”

Risks for infection in patients with asthma (or other atopic conditions): Is asthma more than a chronic airway disease?

“…Two recent studies also showed impaired CMI after nonspecific stimulation in patients with asthma or atopic dermatitis, but antigen-specific CMI was not impaired. 148,149 We recently assessed CMI responses to the viruses in the measles, mumps, and rubella (MMR) vaccine among children aged 12 to 18 years who had received 2 doses of the MMR vaccine. Asthmatic patients with a family history of asthma had significantly poorer CMI responses to MMR vaccine viruses than did those without asthma.…”

Distribution of pathogens causing nosocomial infection in patients with bronchial asthma

“…Otero et al (2013) reported that bacterial infection may elicit the imbalanced expression of T helper cells types 1 and 2 (Koch et al, 2007). Peroni et al (2010) analyzed the pathogen distribution in elderly asthmatic patients and revealed that asthma was induced by the ecological imbalance of pathogenic microbes, which was confirmed by an animal experiment study by Piacentini et al (2010).…”