  Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading
to respiratory failure and subsequent mortality. Sepsis is one of the leading
causes of ARDS. Thus, extracellular bacteria play an important role in the
pathophysiology of ARDS. Overactivated neutrophils are the major effector cells
in ARDS. Thus, extracellular bacteria triggered TH17-like innate immunity with
neutrophil activation might accounts for the etiology of ARDS. Here, microarray
analysis was employed to describe TH17-like innate immunity-related cytokine
including TGF-{\beta} and IL-6 up-regulation in whole blood of ARDS patients.
It was found that the innate TH17-related TLR1,2,4,5,8, HSP70, G-CSF, GM-CSF,
complements, defensin, PMN chemokines, cathepsins, Fc receptors, NCFs, FOS,
JunB, CEBPs, NFkB, and leukotriene B4 are all up-regulated. TGF-{\beta}
secreting Treg cells play important roles in lung fibrosis. Up-regulation of
Treg associated STAT5B and TGF-{\beta} with down-regulation of MHC genes, TCR
genes, and co-stimulation molecule CD86 are noted. Key TH17 transcription
factors, STAT3 and ROR{\alpha}, are down-regulated. Thus, the full adaptive
TH17 helper CD4 T cells may not be successfully triggered. Many fibrosis
promoting genes are also up-regulated including MMP8, MMP9, FGF13, TIMP1,
TIMP2, PLOD1, P4HB, P4HA1, PDGFC, HMMR, HS2ST1, CHSY1, and CSGALNACT. Failure
to induce successful adaptive immunity could also attribute to ARDS
pathogenesis. Thus, ARDS is actually a TH17-like and Treg immune disorder.
