Influence of Microbiota on Clinical Expressions of Respiratory Viral Infections.

Respiratory infections, mainly due to viruses, are among the leading causes of worldwide morbidity and mortality. We investigated the prevalence of viruses and bacteria in a cross-sectional survey conducted in Dielmo, a village in rural Senegal with a population of 481 inhabitants. Nasopharyngeal sampling was performed in 50 symptomatic subjects and 101 asymptomatic subjects. Symptomatic subjects were defined as individuals presenting with clinical signs of respiratory infection, whereas asymptomatic subjects were recruited in the same households. The identification of pathogens was performed by polymerase chain reaction for 18 respiratory viruses and eight respiratory bacteria. The prevalence results for respiratory viruses detected in each study group demonstrated that 83.6% of symptomatic samples were positive for at least one respiratory virus, and 21.8% were detected in asymptomatic samples. Influenza A (P = 0.0001), metapneumovirus (P = 0.04), and enterovirus (P = 0.001) were significantly more prevalent in symptomatic patients. Overall, 82.0% of symptomatic subjects and 26.9% of asymptomatic subjects were positive for at least one respiratory bacterium. The most frequent pathogenic bacteria detected were Moraxella catarrhalis (56%) and Streptococcus pneumoniae (48.0%) among symptomatic individuals, whereas in asymptomatic subjects Corynebacterium propinquum was more prevalent (18%). A principal component analysis showed that parainfluenzas 2 and 4 were associated with asymptomatic subjects, whereas influenza A was associated with the presence of symptoms. Considering these results, a large epidemiological surveillance of the circulation of these respiratory pathogens in the general population should be conducted to provide a better understanding of their carriage and to potentially prevent epidemics.

Imbalance of circulating monocyte subsets and PD-1 dysregulation in Q fever endocarditis: the role of IL-10 in PD-1 modulation.

Q fever endocarditis, a severe complication of Q fever, is associated with a defective immune response, the mechanisms of which are poorly understood. We hypothesized that Q fever immune deficiency is related to altered distribution and activation of circulating monocyte subsets. Monocyte subsets were analyzed by flow cytometry in peripheral blood mononuclear cells from patients with Q fever endocarditis and controls. The proportion of classical monocytes (CD14(+)CD16(-) monocytes) was similar in patients and controls. In contrast, the patients with Q fever endocarditis exhibited a decrease in the non-classical and intermediate subsets of monocytes (CD16(+) monocytes). The altered distribution of monocyte subsets in Q fever endocarditis was associated with changes in their activation profile. Indeed, the expression of HLA-DR, a canonical activation molecule, and PD-1, a co-inhibitory molecule, was increased in intermediate monocytes. This profile was not restricted to CD16(+) monocytes because CD4(+) T cells also overexpressed PD-1. The mechanism leading to the overexpression of PD-1 did not require the LPS from C. burnetii but involved interleukin-10, an immunosuppressive cytokine. Indeed, the incubation of control monocytes with interleukin-10 led to a higher expression of PD-1 and neutralizing interleukin-10 prevented C. burnetii-stimulated PD-1 expression. Taken together, these results show that the immune suppression of Q fever endocarditis involves a cross-talk between monocytes and CD4(+) T cells expressing PD-1. The expression of PD-1 may be useful to assess chronic immune alterations in Q fever endocarditis.