In Vitro Exposure to Escherichia coli Decreases Ion Conductance in the Jejunal Epithelium of Broiler Chickens
Hess M (2014) In Vitro Exposure to Escherichia coli Decreases Ion Conductance in the Jejunal Epithelium of
Broiler Chickens. PLoS ONE 9(3): e92156. doi:10.1371/journal.pone.0092156
In Vitro Exposure to Escherichia coli Decreases Ion Conductance in the Jejunal Epithelium of Broiler Chickens
Wageha A. Awad 0
Claudia Hess 0
Basel Khayal 0
Jo rg R. Aschenbach 0
Michael Hess 0
Markus M. Heimesaat, Charite, Campus Benjamin Franklin, Germany
0 1 Department for Farm Animals and Veterinary Public Health, Clinic for Poultry and Fish Medicine, University of Veterinary Medicine , Vienna , Austria , 2 Institute of Veterinary Physiology, Faculty of Veterinary Medicine, Free University of Berlin , Berlin , Germany
Escherichia coli (E. coli) infections are very widespread in poultry. However, little is known about the interaction between the intestinal epithelium and E. coli in chickens. Therefore, the effects of avian non-pathogenic and avian pathogenic Escherichia coli (APEC) on the intestinal function of broiler chickens were investigated by measuring the electrogenic ion transport across the isolated jejunal mucosa. In addition, the intestinal epithelial responses to cholera toxin, histamine and carbamoylcholine (carbachol) were evaluated following an E. coli exposure. Jejunal tissues from 5-week-old broilers were exposed to 66108 CFU/mL of either avian non-pathogenic E. coli IMT11322 (Ont:H16) or avian pathogenic E. coli IMT4529 (O24:H4) in Ussing chambers and electrophysiological variables were monitored for 1 h. After incubation with E. coli for 1 h, either cholera toxin (1 mg/L), histamine (100 mM) or carbachol (100 mM) were added to the incubation medium. Both strains of avian E. coli (non-pathogenic and pathogenic) reduced epithelial ion conductance (Gt) and short-circuit current (Isc). The decrease in ion conductance after exposure to avian pathogenic E. coli was, at least, partly reversed by the histamine or carbachol treatment. Serosal histamine application produced no significant changes in the Isc in any tissues. Only the uninfected control tissues responded significantly to carbachol with an increase of Isc, while the response to carbachol was blunted to non-significant values in infected tissues. Together, these data may explain why chickens rarely respond to intestinal infections with overt secretory diarrhea. Instead, the immediate response to intestinal E. coli infections appears to be a tightening of the epithelial barrier.
-
E. coli infections in chickens and turkeys are an important
economic threat to the poultry industry worldwide. Although
research has increasingly focused on the pathogenesis of avian
pathogenic Escherichia coli (APEC) infections, little is known about
the reservoirs of these bacteria. Avian pathogenic E. coli (APEC)
are present in the normal microflora of the intestinal tract and
other mucosal surfaces of domestic poultry and wild birds [1]. In
addition, pathogenic serotypes, together with non-pathogenic
serotypes, can be isolated from the birds environment and can
be transmitted to humans [2]. Avian pathogenic E. coli are mostly
associated with extraintestinal disease, principally respiratory or
systemic infections [3,4]. A limited number of serotypes,
principally O1, O2, O78, O8, and O35 are commonly implicated in
avian colibacillosis [5210]. Colibacillosis in mammals is an enteric
disease whereas in poultry it causes localized or systemic disease
occurring mostly when the host defense is impaired. The acute
form of the disease is characterized by septicaemia, resulting in
death, while the subacute form coincides with pericarditis,
airsacculitis and perihepatitis. Infections of the reproductive tract
lead to salpingitis and/or peritonitis with high mortality [11].
The main route for entry of E.coli is the respiratory tract
following inhalation of dust contaminated with feces [12,13].
However, the intestine is the most important reservoir of avian
pathogenic E. coli [14]. The infection strategy of E. coli is to
colonize a mucosal site, evade host defenses and multiply. Poultry
meat contaminated with E. coli may then serves as a possible
reservoir for human infections.
It was shown in a previous study that an Enteropathogenic E.
coli (EPEC) isolated from clinically healthy chickens [11] might
affect the intestinal barrier function in humans [15]. In humans,
EPEC induced a loss of microvillar absorptive surface area
[16,17], and increased epithelial permeability [18220]. E. coli also
altered aquaporin water channel localization and inhibited
sodium, chloride or glucose absorption in human cell culture
[16,21223]. Secretory pathways were also affected by an
enteropathogenic E. coli infection, as alterations in ion transport
have been observed at very early time points in Caco-2 cell
monolayers [24]. Furthermore, E. coli lipopolysaccharide (LPS)
challenge of pigs for 48 h impaired nutrient absorption, increased
permeability in the intestine, decreased tight junction integrity (...truncated)