Serum levels of tumor necrosis factor-α in calves experimentally infected with Pasteurella haemolytica Al

Pace, Lanny W.; Kreeger, John M.; Bailey, Kirstin; Turnquist, Susan E.; Fales, William H.

doi:10.1016/0165-2427(93)90044-5

Cited by 26 publications

(18 citation statements)

References 21 publications

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“…These cytokines promote the production and release of additional proteins, eicosanoids, and free radicals that perpetuate the inflammatory cascade, resulting in severe lung injury (3). There is compelling evidence that inflammatory cytokines play a central role in orchestrating the inflammatory cascade that leads to lung injury in bovine pasteurellosis (15,19,21,22,30,31,35,50,51,52).…”

Section: Discussionmentioning

confidence: 99%

“…One mechanism that might be involved is the release of inflammatory cytokines during viral infection (33,34). Inflammatory cytokines secreted by respiratory tract cells, such as interleukin 1 (IL-1␤), tumor necrosis factor alpha (TNF-␣), and gamma interferon (IFN-␥), can stimulate leukocyte migration and functional activation of ␤ 2 -integrins on lung leukocytes (10,35,38). Once M. haemolytica infection is established in the lung, the continued release of these inflammatory cytokines could be sustained by M. haemolytica virulence factors (i.e., LKT and lipopolysaccharide [LPS]) (15,21,22,30,50,51,52).…”

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Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

et al. 2002

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Mannheimia (Pasteurella) haemolytica A1 is the primary bacterial agent of bovine pneumonic pasteurellosis (shipping fever), which is characterized by acute lobar fibronecrotizing pneumonia with extensive peripheral blood neutrophil (PMN) infiltration in small airways and alveoli (4,39,47). Several virulence factors of M. haemolytica play an important role in the pathogenesis of pasteurellosis (7, 13). Foremost among these is a leukotoxin (LKT), whose effects are specific for ruminant leukocytes and platelets (2, 6, 9, 44). The M. haemolytica LKT is member of the repeats-in-toxin (RTX) family of gram-negative bacterial pore-forming exotoxins (46). Members of the RTX family have similar mechanisms of toxin production, secretion, and target cell intoxication (8, 45). Previously, it has been reported that other members of the RTX family bind to ␤ 2 -integrins on target cells (23). More recently, it has been demonstrated that M. haemolytica LKT binds to lymphocyte function-associated antigen 1 (LFA-1), a ␤ 2 -integrin (CD 11a/CD18) on bovine leukocytes (1,17,25,27). LKT binding to bovine leukocytes induces formation of pore-like structures in the plasma membrane, resulting in both activation of leukocytes and death by necrosis and apoptosis (14,18,24,29,34,40,43,45,53).For reasons that are not well understood, active viral infections can greatly enhance the susceptibility of cattle to M. haemolytica pneumonia (11,28,42,48,49). One mechanism that might be involved is the release of inflammatory cytokines during viral infection (33, 34). Inflammatory cytokines secreted by respiratory tract cells, such as interleukin 1 (IL-1␤), tumor necrosis factor alpha (TNF-␣), and gamma interferon (IFN-␥), can stimulate leukocyte migration and functional activation of ␤ 2 -integrins on lung leukocytes (10,35,38). Once M. haemolytica infection is established in the lung, the continued release of these inflammatory cytokines could be sustained by M. haemolytica virulence factors (i.e., LKT and lipopolysaccharide [LPS]) (15,21,22,30,50,51,52).PMNs are thought to contribute to the lung pathology observed in pneumonic pasteurellosis (4). PMN depletion reduces the severity of lung damage in experimentally infected cattle (4, 39). We hypothesized that inflammatory cytokines released during viral infection might increase surface expression or conformational activation of LFA-1 on bovine PMNs, thus amplifying their interaction with M. haemolytica LKT. In this study, we demonstrated increased expression of LFA-1 on bovine PMNs, as detected by flow cytometry, following incubation of PMNs with IL-1␤, TNF-␣, or IFN-␥. This in turn was reflected in increased LKT binding to, and cytotoxicity for, bovine PMNs. These observations suggest that the ability of inflammatory cytokines to increase surface expression or conformational activation of LFA-1 on bovine PMNs increases their interaction with M. haemolytica LKT. The outcome of the response might increase the severity of bovine pasteurellosis. MATERIALS AND METHODSPMN preparation. Peripheral blood ...

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Section: Discussionmentioning

confidence: 99%

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Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

et al. 2002

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“…LPS activates bovine alveolar macrophage expression and production of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1␤ (IL-1␤), and 37,67,68), all of which are elevated in the lung tissue and bronchoalveolar lavage fluid of cattle affected with shipping fever (8,33,46,68). Moreover, LPS complexes with and seems to act synergistically with Lkt (13, 28).…”

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confidence: 99%

“…During logarithmic growth, the bacteria produce and release a heatlabile exotoxin, termed leukotoxin (Lkt), and a heat-labile enzyme, termed O-sialoglycoprotease (Gcp) (1, 31). Both LPS and Lkt have been implicated in initiating an inflammatory response in cattle in vivo, likely through their activities on leukocytes (20,57,59,65).LPS activates bovine alveolar macrophage expression and production of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1␤ (IL-1␤), and 37,67,68), all of which are elevated in the lung tissue and bronchoalveolar lavage fluid of cattle affected with shipping fever (8,33,46,68). Moreover, LPS complexes with and seems to act synergistically with Lkt (13, 28).…”

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Potential Involvement of Gelatinases and Their Inhibitors inMannheimia haemolyticaPneumonia in Cattle

Starr¹,

Dan²,

Minhas³

et al. 2004

Infect Immun

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Mannheimia haemolytica infection of the lower respiratory tract of cattle results in a bronchofibrinous pneumonia characterized by massive cellular influx and lung tissue remodeling and scarring. Since altered levels of gelatinases and their inhibitors have been detected in a variety of inflammatory conditions and are associated with tissue remodeling, we examined the presence of gelatinases in lesional and nonlesional lung tissue obtained from calves experimentally infected with M. haemolytica. Lesional tissue had elevated levels of progelatinase A and B and active gelatinase A and B when compared with nonlesional tissue obtained from the same lung lobe. In vitro, M. haemolytica products stimulated production of gelatinase B, but not its activation, by bovine monocytes. Alveolar macrophages showed constitutive production of gelatinase B but no change in response to M. haemolytica products. Bovine neutrophils exposed to M. haemolytica products also released gelatinase B, and there was a significant increase in the activated form of this enzyme. These effects were virtually identical when recombinant O-sialoglycoprotease was used to stimulate these cells. M. haemolytica products also enhanced the expression by bovine monocytes and alveolar macrophages of the tissue inhibitor of metalloproteinase 1. Our results provide evidence that matrix metalloproteinases are activated in lung lesions from cattle with shipping fever and that M. haemolytica virulence products induce production, release, and especially activation of gelatinase B by bovine inflammatory cells in vitro.Bronchofibrinous pneumonia (shipping fever) is a respiratory disease in cattle that is characterized by cellular influx and interalveolar and interlobular fibrosis in the lungs of affected animals (3,7,18,20,64,65). Lung lesions consistently show areas of coagulation necrosis, extensive fibrin deposits, and intense cellular infiltration into the alveoli (5, 63, 65). Economic losses to the beef industry due to shipping fever are estimated at over one billion dollars per year in North America alone (64). Causes of this pneumonic condition are multifactorial, including a combination of stress or viral infection, with a final acute illness due most often to the bacteria Mannheimia (Pasteurella) haemolytica serotype A1 (16,39,64). M. haemolytica serotype A1 is a normal resident of the upper respiratory flora of most cattle, but when aspirated into the lower respiratory tract of immunocompromised animals, it is able to colonize the lungs and induce an inflammatory reaction (65).M. haemolytica was originally classified in the genus Pasteurella (50), but more recent genetic characterization has resulted in reclassification of 11 serotypes of biotype A in the new genus Mannheimia (4, 9). M. haemolytica is a trehalosenegative coccobacillus in which heat-stable lipopolysaccharide (LPS) constitutes 12 to 25% of the dried cell wall (66). During logarithmic growth, the bacteria produce and release a heatlabile exotoxin, termed leukotoxin (Lkt), and a heat-labile en...

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“…These virulence factors stimulate a variety of respiratory tract cells such as alveolar and intravascular macrophages, mast cells, and endothelial cells, and these cells express and produce inflammatory mediators. The inflammatory mediators secreted by respiratory tract cells are proinflammatory cytokines (PICs) such as interleukin-1 (IL-1), IL-6, tumor necrosis factor alpha (TNF-␣), complement components, hydrolytic enzymes, and chemokines (20,28,33,38,40,41,48). Once secreted, these inflammatory mediators trigger an inflammatory cascade.…”

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Influence of β₂-Integrin Adhesion Molecule Expression and Pulmonary Infection withPasteurella haemolyticaon Cytokine Gene Expression in Cattle

Lee¹,

Kehrli²,

Brogden

et al. 2000

Infect Immun

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Serum levels of tumor necrosis factor-α in calves experimentally infected with Pasteurella haemolytica Al

Cited by 26 publications

References 21 publications

Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

Potential Involvement of Gelatinases and Their Inhibitors inMannheimia haemolyticaPneumonia in Cattle

Influence of β₂-Integrin Adhesion Molecule Expression and Pulmonary Infection withPasteurella haemolyticaon Cytokine Gene Expression in Cattle

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Serum levels of tumor necrosis factor-α in calves experimentally infected with Pasteurella haemolytica Al

Cited by 26 publications

References 21 publications

Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

Inflammatory Cytokines Enhance the Interaction of Mannheimia haemolytica Leukotoxin with Bovine Peripheral Blood Neutrophils In Vitro

Potential Involvement of Gelatinases and Their Inhibitors inMannheimia haemolyticaPneumonia in Cattle

Influence of β2-Integrin Adhesion Molecule Expression and Pulmonary Infection withPasteurella haemolyticaon Cytokine Gene Expression in Cattle

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Influence of β₂-Integrin Adhesion Molecule Expression and Pulmonary Infection withPasteurella haemolyticaon Cytokine Gene Expression in Cattle