• Neal J Thomas and Joanna Floros.
• Department of Pediatrics, Center for Host defense, Inflammation, and Lung Disease Research, 500 University Drive, H085, Hershey, PA 17033, USA. jfloros@psu.edu
• Crit Care. 2011 Jan 1;15(2):156.

AbstractCommunity-acquired pneumonia is a common disease. Abnormalities in the first step of host defense may severely compromise subsequent steps of successfully combating infections. In the previous issue of Critical Care, García-Laorden and colleagues reported genetic associations between single-nucleotide polymorphisms and haplotypes of the surfactant proteins with susceptibility, severity, and outcome of community-acquired pneumonia. Although the limited information shows regulatory differences among variants, it is currently unknown how the difference in surfactant protein A genotypes in this and other studies affects the individual's phenotype. The lung is continually exposed to a host of irritants yet maintains health. It is plausible that, under physiologic conditions, surfactant protein A, in addition to having a dominant effect on anti-inflammatory processes, mediates a low level of proinflammatory processes that are essential for the health of the lung. Understanding the maintenance of the balance of the inflammatory state may be one of the keys to understanding pulmonary disease progression.

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