Localized pulmonary neutrophil influx induced by lung lavage in sheep

Weiss, Rachelle A.; Chanana, A. D.; Joel, D. D.

doi:10.1007/bf02713886

Cited by 15 publications

(10 citation statements)

References 13 publications

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“…The data presented here suggest that the cellmediated immune response can be limited to not only the lung, but localized areas within the lung. These results are consistent with the localized neutrophil response to bacterial antigens in sheep [26 ] and the IgA response to soluble antigens in monkeys and humans [12,13 ]. Thus, it appears that the T-cell, B-cell, and neutrophil responses to airway antigens can be restricted to localized areas of the lower respiratory tract.…”

Section: Discussionsupporting

confidence: 87%

Angiocentric Recruitment of Lymphocytes Into the Lung After the Intrabronchial Instillation of Antigen

Rawn

DeCamp

Swanson

et al. 2000

Experimental Lung Research

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The pathogenesis of acute lymphocytic inflammation in the lower respiratory tract appears to involve the recruitment of lymphocytes out of the blood stream and into the extravascular lung tissue. To investigate the membrane molecules regulating this process, we used the intrabronchial instillation of cellular antigen to trigger lymphocyte recruitment into the lower respiratory tract. Sheep presensitized 6 to 10 weeks earlier at a remote site were intrabronchially challenged with 1-5 x 10(7) cells from a B lymphoblastoid cell line. The cells were instilled into a subsegmental bronchus through a bronchial catheter. The stimulated and contralateral control segments were studied at a peak of inflammation, approximately 72 hours after antigen stimulation. Gross and microscopic studies of the stimulated segment demonstrated localized inflammation characterized by the perivascular infiltration of lymphocytes. In contrast, control areas of the lung demonstrated only scattered perivascular lymphocytes. Immunohistochemistry of the stimulated lung showed that the majority of these perivascular cells were CD3+ CD4+ lymphocytes. The T lymphocytes expressed high levels of the cell adhesion molecules beta 1 integrin and LFA-1, but low levels of the L-selectin membrane molecule. Immunohistochemistry of the endothelial cells associated with the lymphocyte infiltrates demonstrated intense staining of the ICAM-1, and beta 1 integrin adhesion molecules. Electron microscopic studies of the endothelial cells in the antigen stimulated areas of the lung confirmed morphologic changes consistent with endothelialitis. These results suggest that the intrabronchial instillation of cellular antigen stimulates an angiocentric T-cell infiltration regulated by activated pulmonary endothelial cells. The histologic and morphologic findings are remarkably similar to those observed during acute lung transplant rejection.

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Section: Discussionsupporting

confidence: 87%

Angiocentric Recruitment of Lymphocytes Into the Lung After the Intrabronchial Instillation of Antigen

Rawn

DeCamp

Swanson

et al. 2000

Experimental Lung Research

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“…Treatment with PBS alone resulted in a high percentage of neutrophils recovered in the BAL fluid. This effect of liquid instillation in the lung has been shown to occur in other studies in which lavage with sterile saline solution in vivo induces an inflammatory response in the lungs characterized by an influx of neutrophils in a number of animal species [39][40][41] and in humans [42]. However, the inflammatory response induced by PBS was less than that of CSE made in PBS, as seen with RPMI and CSE made with RPMI.…”

Section: Discussionmentioning

confidence: 53%

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Elliott

Sisson

West

et al. 2006

Experimental Lung Research

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In this study the authors compared the affect of vapor phase cigarette smoke (CS) versus cigarette smoke extract (CSE) on the lungs and upper airway of C57BL/6 mice. The authors found that CSE treatment significantly increased neutrophil influx (P < .001), baseline ciliary beat frequency (CBF) (P < .05), and protein kinase C activity compared to CS and controls. Isoproterenol increased CBF with CS exposure, but decreased CBF with CSE (P < .01). Isoproterenol increased protein kinase A (PKA) activity in all groups except CSE. CSE exposure induced inflammatory cell bronchiolitis. These data indicate that CSE exposure has differential effects on the lungs and tracheal epithelium compared to CS exposure.Ciliary motility provides the driving force for mucociliary clearance. Normal function of the airway mucociliary clearance system prevents the attachment and colonization of pulmonary pathogens in the upper airways. Mucociliary dysfunction caused by impaired ciliary motility results in mucus accumulation, airway obstruction, and bacterial colonization, increasing the likelihood of infection in the lower airway [1][2][3]. Mucociliary clearance is affected by exposure to a number of environmental agents [4,5], including cigarette smoke. Exposure to cigarette smoke (CS) has been linked to the development of lung cancer, emphysema, chronic bronchitis, and chronic obstructive pulmonary disease (COPD) [6]. Smokers are at a higher risk for pulmonary infection [7]. Chronic exposure to tobacco smoke is associated with increased ciliary abnormality [8] and reduced mucociliary clearance [9]. The increased risk for infection seen in smokers may be due to alterations in ciliary function in the upper airway.Several studies have revealed that ciliary activity is controlled by phosphorylation of axonemal proteins [10][11][12]. Protein kinase C (PKC) and cyclic adenosine monophosphate (CAMP)-Address correspondence to Todd A. Wyatt, PhD, University of Nebraska Medical Center, 985300 Nebraska Medical Center, Omaha, NE 68198-5300, USA. E-mail: twyatt@unmc.edu. NIH Public Access Author ManuscriptExp Lung Res. Author manuscript; available in PMC 2007 November 21. Published in final edited form as:Exp Lung Res. 2006 ; 32(3-4): 99-118. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript dependent protein kinase (PKA) are important regulators of airway ciliary beat frequency (CBF). Agents that increase PKC are associated with decreased CBF [13][14][15]. Alternatively, agents associated with increased CBF also increase PKA activity [16]. In past studies, we have shown that exposure of ciliated epithelial cells to cigarette smoke extract (CSE) in culture and whole cigarette smoke in vivo induces an increase in epithelial cell PKC activity [15,[17][18][19]. Many animal models of exposure to cigarette smoke components exist. Most recently, Miller and colleagues have developed a method of exposure consisting of intranasal administration of CSE [20]. This method was shown to induce an inflammatory response similar to ...

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“…Also, the slight irritation and inflammatory reaction produced by the bronchoscopy and a single bronchoalveolar lavage procedure can initiate the granulocyte invasion, especially in the case of repeated lavage procedures of the same bronchial segment, as described by Weiss et al (23). In contrast, only the d-segments contained normal granulocyte/alveolar macrophage ratio in the lavage fluid after endotoxin injection for up to seven lavage procedures of the same animal within an 8 hour period.…”

Section: Discussionmentioning

confidence: 88%

Alveolar Cell Pattern and Chemiluminescence Response of Blood Neutrophils and Alveolar Macrophages in Sheep after Endotoxin Injection

Dwenger

Regel²,

Ellendorff³

et al. 1990

Clinical Chemistry and Laboratory Medicine

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In order to study the pathomechanisms of the Adult Respiratory Distress Syndrome in an acute animal model, we monitored the alveolar cell pattern and the stimulatory chemiluminescence responses of blood neutrophils and alveolar macrophages in sheep after Escherichia coli endotoxin injection (2 g/kg of body weight). Using appropriate bronchoalveolar lavage techniques, thereby avoiding local inflammation, it was demonstrated that endotoxin injection did not cause any recruitement of neutrophils into the alveoli for a period of up to 24 hours. Following endotoxin injection, blood neutrophils showed a maximal stimulatory response after 5 minutes, and alveolar macrophages after 4 hours. It is concluded that if neutrophils are responsible for initiating the increase in microvascular permeability, then this action must be purely intravascular.

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Localized pulmonary neutrophil influx induced by lung lavage in sheep

Cited by 15 publications

References 13 publications

Angiocentric Recruitment of Lymphocytes Into the Lung After the Intrabronchial Instillation of Antigen

Angiocentric Recruitment of Lymphocytes Into the Lung After the Intrabronchial Instillation of Antigen

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Alveolar Cell Pattern and Chemiluminescence Response of Blood Neutrophils and Alveolar Macrophages in Sheep after Endotoxin Injection

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