Acid aspiration induces bacterial pneumonia by enhanced bacterial adherence in mice

Mitsushima, Hiroaki; Oishi, Kazunori; Nagao, Takayoshi; Ichinose, Akitoyo; Senba, Masachika; Iwasaki, Takuya; Nagatake, Tsuyoshi

doi:10.1006/mpat.2002.0529

Cited by 31 publications

(30 citation statements)

References 24 publications

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“…However, the rats treated with HCl and LPS at 20 or 30 g/g body wt had a lower and more acceptable mortality rate (ϳ20%), and lower than that in other models of aspiration pneumonia using live bacteria (18,23,27). Also, there was a remarkable loss of total body weight in the first 24 h in all rats treated with HCl/LPS.…”

Section: Discussionmentioning

confidence: 83%

“…Taken into account that HCl is rapidly neutralized in the lung (3), we instilled LPS as a second hit two hours after instillation of HCl in order to enhance lung injury. In previous studies, different intervals of time between instillations of HCl (or gastric aspirate) and LPS (or live bacteria) have been used, ranging from few minutes (23,27) to 16 -24 h (18, 30, 32). In all cases, the instilled HCl (or gastric aspirate) primes the host to enhance acute inflammatory responses to a subsequent administration of LPS or live bacteria.…”

Section: Discussionmentioning

confidence: 99%

“…However, to our knowledge, only a few experimental studies have investigated the pathogenesis of pneumonia in the host with aspiration pneumonitis (18,23,27,30,32). These previous studies have shown that aspiration of gastric acid strongly enhances pulmonary inflammation induced by lipopolysaccharide (LPS) (32) or bacteria (18,30).…”

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confidence: 99%

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A new experimental model of acid- and endotoxin-induced acute lung injury in rats

Puig

Herrero

Guillamat-Prats

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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-The majority of the animal models of acute lung injury (ALI) are focused on the acute phase. This limits the studies of the mechanisms involved in later phases and the effects of long-term treatments. Thus the goal of this study was to develop an experimental ALI model of aspiration pneumonia, in which diffuse alveolar damage continues for 72 h. Rats were intratracheally instilled with one dose of HCl (0.1 mol/l) followed by another instillation of one dose of LPS (0, 10, 20, 30, or 40 g/g body weight) 2 h later, which models aspiration of gastric contents that progresses to secondary lung injury from bacteria or bacterial products. The rats were euthanized at 24, 48, and 72 h after the last instillation. The results showed that HCl and LPS at all doses caused activation of inflammatory responses, increased protein permeability and apoptosis, and induced mild hypoxemia in rat lungs at 24 h postinstillation. However, this lung damage was present at 72 h only in rats receiving HCl and LPS at the doses of 30 and 40 g/g body wt. Mortality (ϳ50%) occurred in the first 48 h and only in the rats treated with HCl and LPS at the highest dose (40 g/g body wt). In conclusion, intratracheal instillation of HCl followed by LPS at the dose of 30 g/g body wt results in severe diffuse alveolar damage that continues at least 72 h. This rat model of aspiration pneumonia-induced ALI will be useful for testing long-term effects of new therapeutic strategies in ALI.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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A new experimental model of acid- and endotoxin-induced acute lung injury in rats

Puig

Herrero

Guillamat-Prats

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Originally described in women during labor and in perioperative patients (6,7), aspiration occurs when gastric or oropharyngeal contents inadvertently gain access into the lower respiratory tract. Below a threshold pH, gastric acid causes airway injury and can predispose to bacterial pneumonia owing to transient disruption in mucosal host defense mechanisms (8)(9)(10)(11).No matter the cause, in most instances, pneumonia spontaneously resolves (12), suggesting the existence of endogenous, host-protective signaling pathways. Despite carefully detailing the remarkable histopathologic events that return the architecture of the lung from complete consolidation to a seemingly normal state (13), there is only a limited understanding of the mechanisms underlying this process of resolution from lung infection.…”

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confidence: 99%

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confidence: 99%

The Anti-inflammatory And Pro-resolving Mediator Resolvin E1 Protects Mice From Bacterial Pneumonia And Acute Lung Injury

Seki¹,

Fukunaga²,

Arita³

et al. 2010

A34. Lung Injury: Mechanism and Interventions

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Whereas pneumonia is the most common cause of death and disability worldwide, most cases of pneumonia spontaneously resolve. Mechanisms that promote pneumonia resolution remain to be determined. Resolvin E1(RvE1) is an endogenous mediator that displays proresolving actions in sterile inflammation. In this study, we developed a new model of aspiration pneumonia to evaluate the effect of RvE1 on acute lung injury caused by acid aspiration and subsequent bacterial challenge. Mice received hydrochloric acid into the left lung followed by the enteric pathogen Escherichia coli. I.v. administration of RvE1 (~0.005 mg/kg) prior to acid injury selectively decreased lung neutrophil accumulation by 55% and enhanced clearance of E. coli. RvE1 significantly decreased lung tissue levels of several proinflammatory chemokines and cytokines, including IL-1β, IL-6, HMGB-1, MIP-1α, MIP-1β, keratinocyte-derived chemokine, and MCP-1, in a manner independent of the anti-inflammatory mediators IL-10 and lipoxin A 4 . In addition, animals treated with RvE1 had a marked improvement in survival. These findings in experimental aspiration pneumonia have uncovered protective roles for RvE1 in pathogen-mediated inflammation that are both anti-inflammatory for neutrophils and protective for host defense, Copyright © 2009 suggesting that RvE1 represents the first candidate for a novel therapeutic strategy for acute lung injury and pneumonia that harnesses natural resolution mechanisms.More than any other infection, acute pneumonia causes the greatest morbidity and mortality (1). To address the important global unmet need for treatment (2), several new antibiotics were developed over the last several decades, yet pneumonia mortality has not decreased (1,3). One explanation for the persistent adverse outcomes for pneumonia is the pathogeninitiated inflammatory response that can spiral out of control and lead to acute lung injury (ALI) or the acute respiratory distress (ARDS) (4). Whereas pathogen-mediated inflammation is essential for host defense, unrestrained activation of leukocytes and lung tissue resident cells can lead to excess tissue injury (5) and in the case of pneumonia, subsequent hypoxemia. New insights are needed to provide new therapeutic approaches.Aspiration pneumonia is one of the leading causes of pneumonia and ALI/ARDS (4). Originally described in women during labor and in perioperative patients (6,7), aspiration occurs when gastric or oropharyngeal contents inadvertently gain access into the lower respiratory tract. Below a threshold pH, gastric acid causes airway injury and can predispose to bacterial pneumonia owing to transient disruption in mucosal host defense mechanisms (8)(9)(10)(11).No matter the cause, in most instances, pneumonia spontaneously resolves (12), suggesting the existence of endogenous, host-protective signaling pathways. Despite carefully detailing the remarkable histopathologic events that return the architecture of the lung from complete consolidation to a seemingly normal state (13), there ...

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Infectious Disease

Simon¹,

Sarkar²

2021

Canine and Feline Anesthesia and Co‐Existing Disease

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Acid aspiration induces bacterial pneumonia by enhanced bacterial adherence in mice

Cited by 31 publications

References 24 publications

A new experimental model of acid- and endotoxin-induced acute lung injury in rats

A new experimental model of acid- and endotoxin-induced acute lung injury in rats

The Anti-inflammatory And Pro-resolving Mediator Resolvin E1 Protects Mice From Bacterial Pneumonia And Acute Lung Injury

Infectious Disease

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