Efecto del lipopolisacárido (LPS) de E. coli sobre la cantidad de células caliciformes, leucocitos y sobre la distribución de mucinas en el pulmón de cerdos postdestete

Abstract

RESUMEN: El periodo postdestete en los cerdos está caracterizado por una serie de alteraciones orgánicas de tipo estructurales y funcionales, que predisponen al desarrollo de enfermedades entéricas y del tracto respiratorio. Un agente patógeno importante en este periodo es la Escherichia coli, una bacteria gram negativa que posee en su pared celular lipopolisacárido (LPS), factor patogénico importante en la presentación de procesos endotóxicos e importante activador de la respuesta inmune innata. Actualmente se desconoce el efecto de LPS sobre la distribución de mucinas en el tracto respiratorio de los cerdos y su relación con la presentación de procesos inflamatorios en el pulmón. Objetivo: determinar el efecto del LPS de E. coli sobre la distribución de las mucinas en el pulmón de lechones postdestete. Además se espera establecer el efecto de LPS sobre la respuesta leucocitaria. Metodología: Para este estudio se utilizaron tejidos incluidos en parafina obtenidos de una investigación anterior que se encuentran almacenados en el Laboratorio de Patología Animal de la Universidad de Antioquia. Las muestras se obtuvieron en un estudio experimental previo que se realizó con 52 lechones destetados a los 21 días de edad. Los animales fueron alimentados con una dieta basal adicionada con cuatro niveles de LPS (0.0, 0.3, 0.5 y 1.0 ug/mg de alimento) durante 10 días. Los cerdos se sacrificaron escalonadamente los días 1, 5, 7 y 10 postdestete y se tomaron muestras de pulmón.

ABSTRACT: The postweaning period in pigs is characterized by a series of organic alterations of functional and structural type, which predispose to the development of enteric and respiratory tract diseases. An important pathogen in this period is the Escherichia coli, a gram-negative bacterium that has in its cell wall lipopolysaccharide (LPS), which is an important pathogenic factor in endotoxic processes and a potent activator of the innate immune response. The effect of LPS on the mucin distribution in the respiratory tract of pigs and their relationship with the presentation of inflammatory processes in the lung is unknown. Objective: To determine the effect of LPS of E. coli on the distribution of mucins in the lung of piglets after weaning. It is also expected to establish the effect of LPS on leukocyte response. Methodology: For this study, paraffin-embedded tissues obtained from a previous study were used. These tissues were stored at the Laboratory of Animal Pathology, University of Antioquia. The samples were obtained in a previous experimental study conducted with 52 piglets weaned at 21 days of age. The animals were fed a basal diet supplemented with four levels of LPS (0.0, 0.3, 0.5 and 1.0 ug / mg of food) for 10 days. Pigs were sacrificed stepwise days 1, 5, 7 and 10 post-weaning and lung samples were taken. In these samples, histological sections were made with a thickness of 4 um and histochemical stainings were performed to determine the number of goblet cells expressing neutral and acid mucins and the type of leukocyte infiltration, using a computerized image analysis. For statistical analysis the random block design was used on a 4 x 4 factorial arrangement. Results and discussion: In control piglets was observed a decrease in the number of goblet cells in bronchi and bronchioles, with a recovery of values for the tenth day, the LPS inhibited this recovery of this cell line and neutral mucins produced by them. In all experimental units increased acidic mucin in the bronchi on day 5 postweaning and no acidic mucins were observed in their bronchioles. In addition the higher concentrations of LPS caused a decrease in the number of neutrophils on day tenth and no effects on the amount of other leukocytes. Conclusions: LPS affects the recovery of goblet cells in the airway epithelium of the lung and decreases the number of neutrophils, altering the innate immunity in early weaning, which may favor the entry of pathogens and allergen sensitization.