Endotoxin induced peritonitis elicits monocyte immigration into the lung: implications on alveolar space inflammatory responsiveness

Steinmüller, Mirko; Srivastava, Mrigank; Kuziel, William A.; Christman, John W.; Seeger, Werner; Welte, Tobias; Lohmeyer, Jürgen; Maus, Ulrich A.

doi:10.1186/1465-9921-7-30

Cited by 20 publications

(19 citation statements)

References 17 publications

(53 reference statements)

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“…The data of Steinmüller and colleagues showed that, in mice, the intraperitoneal endotoxin triggers the recruitment not only of granulocytes, but also of monocytes into the lungs, which amplifies the lung inflammatory responses with a "second-hit" endotoxin challenge intratracheally [44]. In our study, we injected LPS endotoxin intraperitoneally, but, in contrast of previous models, signs of septic shock syndrome could not be observed either clinically or histopathologically.…”

Section: Baltcontrasting

confidence: 83%

Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Bánfi¹,

Tiszlavicz

Székely³

et al. 2009

Experimental Lung Research

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Gram-negative bacterial endotoxin lipopolysaccharide (LPS) administration has been used as an animal model of sepsis-related acute lung injury and adult respiratory distress syndrome (ALI/ARDS). This paper describes the lung histology following lung injury induced by the intraperitoneal (i.p.) administration of endotoxin to rats, in comparison with earlier findings. ALI was induced by the i.p. administration of Esherichia coli LPS 2 (n = 8) or 3 (n = 5) mg/kg, whereas physiological saline was administered to the control animals (n = 5). Eighteen hours after the LPS injections, the animals were euthanized. The lungs and heart were removed in one block for histological study (hematoxylin and eosin [H&E], periodic acid-Schiff [PAS], Mason's trichrome; light microscopy). The lung tissue injury (bronchial wall, vessels, alveoli, interstitium) was graded via a scoring system (0 to 3+). The control animals showed intact lung tissue. Ten of the 13 LPS group had bronchus-associated lymphoid tissue (BALT) hyperplasia. Pathological signs of ALI/ARDS, diffuse alveolar damage (DAD) and emphysema, were observed in 5 and 8 cases, respectively. LPS injection induces primarily BALT hyperplasia and also the less characteristic DAD. This rat model is suitable for the investigation not only of ALI/ARDS but also of BALT hyperplasia occurring as a consequence of chronic pulmonary inflammatory processes.

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Section: Baltcontrasting

confidence: 83%

Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Bánfi¹,

Tiszlavicz

Székely³

et al. 2009

Experimental Lung Research

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“…Although i.p. injections of LPS also evoke acute lung injury, the pulmonary responses of animal (e.g., BAL fluid cytokine/chemokine profiles and BAL fluid cellular constituents) are different due to different LPS approaches (22,23). We cannot find reports on the use of a selective Src TK inhibitor, PP1, in i.t.…”

Section: N Uclear Factor B (Nf-b) Is Transcriptional Regulatorymentioning

confidence: 89%

Src Tyrosine Kinases Mediate Activations of NF-κB and Integrin Signal during Lipopolysaccharide-Induced Acute Lung Injury

Lee

Moon

Lee

et al. 2007

The Journal of Immunology

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Src tyrosine kinases (TKs) are signaling proteins involved in cell signaling pathways toward cytoskeletal, membrane and nuclear targets. In the present study, using a selective Src TK inhibitor, PP1, we investigated the roles of Src TKs in the key pulmonary responses, NF-κB activation, and integrin signaling during acute lung injury in BALB/C mice intratracheally treated with LPS. LPS resulted in c-Src phosphorylation in lung tissue and the phospho-c-Src was predominantly localized in recruited neutrophils and alveolar macrophages. PP1 inhibited LPS-induced increases in total protein content in bronchoalveolar lavage fluid, neutrophil recruitment, and increases in the production or activity of TNF-α and matrix metalloproteinase-9. PP1 also blocked LPS-induced NF-κB activation, and phosphorylation and degradation of IκB-α. The inhibition of NF-κB activation by PP1 correlated with a depression of LPS-induced integrin signaling, which included increases in the phosphorylations of integrin β3, and of the focal adhesion kinase (FAK) family members, FAK and Pyk2, in lung tissue, and reductions in the fibrinogen-binding activity of alveolar macrophages. Moreover, treatment with anti-αv, anti-β3, or Arg-Gly-Asp-Ser (RGDS), inhibited LPS-induced NF-κB activation. Taken together, our findings suggest that Src TKs play a critical role in LPS-induced activations of NF-κB and integrin (αvβ3) signaling during acute lung injury. Therefore, Src TK inhibition may provide a potential means of ameliorating inflammatory cascade-associated lung injury.

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“…It is generally held that monocytes/ macrophages play a central role in the host response against bacterial infections, although the published data on the role of monocytes/macrophages for pulmonary neutrophilia are complex and contradictory. For example, on the one hand, one study (35) reported that alveolar macrophages are a positive regulator endotoxin-induced neutrophil accumulation in the lung. On the other hand, another study (2) has shown that depletion of alveolar macrophages has no effect or even increases pulmonary recruitment of neutrophils in response to endotoxin (2).…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophils are particularly sensitive to C-X-C motif (CXC) chemokines, including chemokine CXC ligand (CXCL)1, CXCL2, and CXCL5 (20). Although it is widely held that monocytes play an important role in systemic inflammation, the literature on the role of monocytes in controlling pulmonary neutrophilia is complex and partly contradictory (1,35). Thus, we decided to examine the role of blood monocytes for pulmonary accumulation of neutrophils as well as cytokine and chemokine formation in abdominal sepsis.…”

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confidence: 99%

Monocytes regulate systemic coagulation and inflammation in abdominal sepsis

Wang

Braun

Zhang

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Wang Y, Braun OÖ, Zhang S, Norström E, Thorlacius H. Monocytes regulate systemic coagulation and inflammation in abdominal sepsis. Am J Physiol Heart Circ Physiol 308: H540-H547, 2015. First published December 12, 2014; doi:10.1152/ajpheart.00336.2014.-Abdominal sepsis is associated with significant changes in systemic inflammation and coagulation. The purpose of the present study was to examine the role of peripheral blood monocytes for systemic coagulation, including thrombin generation and consumption of coagulation factors. Abdominal sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice. Plasma and lung levels of IL-6 and C-X-C motif (CXC) chemokines [chemokine CXC ligand (CXCL)1, CXCL2, and CXCL5], pulmonary activity of myeloperoxidase, thrombin generation, and coagulation factors were determined 6 h after CLP induction. Administration of clodronate liposomes decreased circulating levels of monocytes by 96%. Time to peak thrombin formation was increased and peak and total thrombin generation was decreased in plasma from CLP animals. Monocyte depletion decreased time to peak formation of thrombin and increased peak and total generation of thrombin in septic animals. In addition, monocyte depletion decreased the CLP-induced increase in the levels of thrombin-antithrombin complexes in plasma. Depletion of monocytes increased plasma levels of prothrombin, factor V, factor X, and protein C in septic mice. Moreover, depletion of monocytes decreased CLP-induced levels of IL-6 and CXC chemokines in the plasma and lung by Ͼ59% and 20%, respectively. CLP-induced myeloperoxidase activity in the lung was attenuated by 44% in animals depleted of monocytes. Taken together, our findings show, for the first time, that peripheral blood monocytes regulate systemic coagulation. The results of our study improve our understanding of the pathophysiology of sepsis and encourage further attempts to target innate immune cell functions in abdominal sepsis. coagulation; innate immunity; inflammation; sepsis; thrombin ABDOMINAL SEPSIS is a leading cause of hospital-related deaths (3, 16). Sepsis-induced mortality ranges between 18% and 30%, and the presence of disseminated intravascular coagulation increases the mortality rate to 35% (8, 13, 31). The high mortality rate in septic patients is in part related to an incomplete understanding of the underlying pathophysiology. Intestinal contamination of the abdominal cavity with toxins and microbes causes local formation of proinflammatory substances, such as cytokines and chemokines (18). Translocation of microbes, toxins, and proinflammatory substances into the circulation triggers a systemic inflammatory response characterised by widespread activation of innate immune cells, such as monocytes and neutrophils, leading to organ injury (5, 28). Several studies have shown that pulmonary recruitment of neutrophils is a rate-limiting step in septic lung injury (9, 11). Neutrophils are particularly sensitive to C-X-C motif (CXC) chemokines, including chemokine CXC ligand (CX...

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Endotoxin induced peritonitis elicits monocyte immigration into the lung: implications on alveolar space inflammatory responsiveness

Cited by 20 publications

References 17 publications

Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Development of Bronchus-Associated Lymphoid Tissue Hyperplasia Following Lipopolysaccharide-Induced Lung Inflammation in Rats

Src Tyrosine Kinases Mediate Activations of NF-κB and Integrin Signal during Lipopolysaccharide-Induced Acute Lung Injury

Monocytes regulate systemic coagulation and inflammation in abdominal sepsis

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