Interactions of Histophilus somni with Host Cells

Abstract

Histophilus somni resides as part of the normal microflora in the upper respiratory tract of healthy cattle. From this site, the organism can make its way into the lower respiratory tract, where it is one of the important bacterial agents of the respiratory disease complex. If H. somni cells disseminate to the bloodstream, they frequently result in thrombus formation. A series of in vitro investigations have examined potential mechanisms that might contribute to such thrombus formation. Earlier work showed that H. somni can stimulate some bovine endothelial cells to undergo apoptosis. More recent studies indicate that H. somni stimulates endothelial cell tissue factor activity and disrupts intercellular junctions. The net effect is to enhance procoagulant activity on the endothelium surface and to make the endothelial monolayer more permeable to molecules, leukocytes, and perhaps H. somni cells. H. somni also activates bovine platelets, which also can enhance tissue factor activity on the endothelium surface. When exposed to H. somni, bovine neutrophils and mononuclear phagocytes form extracellular traps in vitro. Ongoing research is investigating how the interplay among endothelial cells, platelets, and leukocytes might contribute to the thrombus formation seen in infected cattle.

An overview of the detection of bovine respiratory disease complex pathogens using immunohistochemistry: emerging trends and opportunities

“…7 Similarly, in H. somni –infected lung tissues, IHC was utilized to visualize and locate bacteria in endothelial cells, 24 neutrophils, and macrophages. 5 The use of IHC to determine the presence of H. somni in the respiratory tract of cattle with BRDC has been crucial for assessing the interaction between H. somni and host cells and for understanding the pathogenesis of BRDC.…”

Histophilus somni Survives in Bovine Macrophages by Interfering with Phagosome-Lysosome Fusion but Requires IbpA for Optimal Serum Resistance

“…Virulent strains of H. somni possess a wide variety of physiological properties and mechanisms that enable the bacteria to resist the bactericidal effects of host defenses or to modulate host immune cells. Such mechanisms include phase variation of lipooligosaccharide (LOS), modification of LOS with sialic acid and phosphorylcholine (4), apoptosis of endothelial cells and neutrophils with disruption of intercellular junctions (5), and biofilm formation (6). Furthermore, the bacteria secrete a fibrillar and surface-associated immunoglobulin binding protein (IbpA), the N-terminal region of which is capable of binding immunoglobulins through their Fc component and may also contribute to the adherence of the bacteria to host cells (7).…”

Histophilus somniSurvives in Bovine Macrophages by Interfering with Phagosome-Lysosome Fusion, but Requires IbpA for Optimal Serum Resistance

“…Virulent strains of H. somni possess a wide variety of physiological properties and mechanisms that primarily protect the bacteria from host defenses or modulate host immune cells. Such mechanisms include phase variation of lipooligosaccharide (LOS), modification of LOS with sialic acid and phosphorylcholine (4), apoptosis of endothelial cells and neutrophils with disruption of intercellular junctions (5), and biofilm formation (6). Furthermore, the bacteria secrete a fibrillar and surface-associated immunoglobulin binding protein (IbpA), of which the N -terminus region is capable of binding immunoglobulins through their Fc component, and may also mediate adherence of the bacteria to host cells (7).…”