The Acute Inflammatory Response and Its Regulation

RNA expression patterns change dramatically in human neutrophils exposed to bacteria

“…Ligated cDNA was amplified by PCR with a phosphorous 32 ( 32 P)-labeled primer complementary to one arm of the Y-shaped adapter and a second primer complementary to the oligo-dT primer and containing one of the 12 possible dinucleotide extensions on its 3Ј-end, as previously described. 1,2 Ec indicates E coli K12; Yp (KIM5), Y pestis KIM5 (pCD1 ϩ ); Yp (KIM6), Y pestis KIM6 (pCD1 Ϫ ); N, neutrophil; and M, monocyte. Gene symbols are the same as those described in Tables 4-6, except for the following: PAI2, plasminogen activator inhibitor, type II (arginine-serpin) (GenBank Accession no.…”

“…Neutrophils are the first cells to be recruited from the blood stream to sites of inflammation 1,2 and are critically important for determining the outcome of some acute infections. 3 They are postmitotic cells that synthesize lower levels of protein and RNA than most dividing cells, and they can interact and/or modulate inflammation.…”

Neutrophils: Molecules, Functions and Pathophysiological Aspects

“…T he notion that inflammation is the net resultant of pro and contra inflammatory pathways (Fauve, 1980) is well illustrated by the dual role of neutrophils which combine an anti-infectious and a proinflammatory role (Klebanoff, 1992;Ward, 1999;Weiss, 1989). The aim of this report is to review the main physiological and pathogenic activities of neutrophils-ie, adherence and migration, degranulation and release of inflammatory mediators, phagocytosis and apoptosis-in the light of the most recent molecular data on extracellular effectors and regulators, membrane receptors, and intracellular signaling pathways involved in these functions.…”

Differential Effects of CD18, CD29, and CD49 Integrin Subunit Inhibition on Neutrophil Migration in Pulmonary Inflammation

“…This process of migration has many stages and is regulated at each by a range of inflammatory mediators (for reviews, see Refs. [5][6][7]. The onset of inflammation results in increased expression, or altered avidity of adhesion molecules, and thus increases the adhesiveness of both the circulating cells and the endothelium (for reviews, see Refs.…”