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    Individual-level Association of Influenza Infection With Subsequent Pneumonia: A Case-control and Prospective Cohort Study. Kubale John,Kuan Guillermina,Gresh Lionel,Ojeda Sergio,Schiller Amy,Sanchez Nery,Lopez Roger,Azziz-Baumgartner Eduardo,Wraith Steph,Harris Eva,Balmaseda Angel,Zelner Jon,Gordon Aubree Clinical infectious diseases : an official publication of the Infectious Diseases Society of America BACKGROUND:Pneumonia is a leading cause of mortality worldwide. Influenza may result in primary pneumonia or be associated with secondary bacterial pneumonia. While the association with secondary pneumonia has been established ecologically, individual-level evidence remains sparse and the risk period for pneumonia following influenza poorly defined. METHODS:We conducted a matched case-control study and a prospective cohort study among Nicaraguan children aged 0-14 years from 2011 through 2018. Physicians diagnosed pneumonia cases based on Integrated Management for Childhood Illness guidelines. Cases were matched with up to 4 controls on age (months) and study week. We fit conditional logistic regression models to assess the association between influenza subtype and subsequent pneumonia development, and a Bayesian nonlinear survival model to estimate pneumonia hazard following influenza. RESULTS:Participants with influenza had greater risk of developing pneumonia in the 30 days following onset compared to those without influenza (matched odds ratio [mOR], 2.7 [95% confidence interval {CI}, 1.9-3.9]). Odds of developing pneumonia were highest for participants following A(H1N1)pdm09 illness (mOR, 3.7 [95% CI, 2.0-6.9]), followed by influenza B and A(H3N2). Participants' odds of pneumonia following influenza were not constant, showing distinct peaks 0-6 days (mOR, 8.3 [95% CI, 4.8-14.5] days) and 14-20 (mOR, 2.5 [95% CI, 1.1-5.5] days) after influenza infection. CONCLUSIONS:Influenza is a significant driver of both primary and secondary pneumonia among children. The presence of distinct periods of elevated pneumonia risk in the 30 days following influenza supports multiple etiological pathways. 10.1093/cid/ciaa1053
    IL-17 production by tissue-resident MAIT cells is locally induced in children with pneumonia. Lu Bingtai,Liu Ming,Wang Jun,Fan Huifeng,Yang Diyuan,Zhang Li,Gu Xiaoqiong,Nie Junli,Chen Zhenjun,Corbett Alexandra J,Zhan Michael J,Zhang Shengbo,Bryant Vanessa L,Lew Andrew M,McCluskey James,Luo Hai-Bin,Cui Jun,Zhang Yuxia,Zhan Yifan,Lu Gen Mucosal immunology Community-acquired pneumonia (CAP) contributes substantially to morbidity and mortality in children under the age of 5 years. In examining bronchoalveolar lavages (BALs) of children with CAP, we found that interleukin-17 (IL-17) production was significantly increased in severe CAP. Immune profiling showed that mucosal-associated invariant T (MAIT) cells from the BALs, but not blood, of CAP patients actively produced IL-17 (MAIT17). Single-cell RNA-sequencing revealed that MAIT17 resided in a BAL-resident PLZFCD103 MAIT subset with high expression of hypoxia-inducible factor 1α (HIF-1α), reflecting the hypoxic state of the inflamed tissue. CAP BALs also contained a T-bet MAIT1 subset and a novel DDIT3 (DNA damage-inducible transcript 3-positive) MAIT subset with low expression of HIF1A. Furthermore, MAIT17 differed from T-helper type 17 (Th17) cells in the expression of genes related to tissue location, innateness, and cytotoxicity. Finally, we showed that BAL monocytes were hyper-inflammatory and elicited differentiation of MAIT17. Thus, tissue-resident MAIT17 cells are induced at the infected respiratory mucosa, likely influenced by inflammatory monocytes, and contribute to IL-17-mediated inflammation during CAP. 10.1038/s41385-020-0273-y