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Background   Actinobacillus pleuropneumoniae  causes contagious pleuropneumonia, an economically important disease of commercially reared pigs throughout the world. To cause this disease,  A. pleuropneumoniae  must rapidly overcome porcine pulmonary innate immune defenses. Since bronchoalveolar fluid (BALF) contains many of the innate immune and other components found in the lungs, we examined the gene expression of a virulent serovar 1 strain of  A. pleuropneumoniae  after exposure to concentrated BALF for 30 min.    Results  In reverse transcription PCR differential display (RT-PCR DD) experiments,  A. pleuropneumoniae  CM5 exposed to BALF up-regulated, among other genes, a gene predicted to encode LamB, an outer-membrane transport protein of the maltose regulon. To determine the role of the  lamB  and other genes of the maltose regulon in the pathogenesis of  A. pleuropneumoniae , knockout mutations were created in the  lamB  and  malT  genes, the latter being the positive transcriptional regulator of the maltose regulon. Relative to the  lamB  mutant and the wild type, the  malT  mutant had a significant ( P  < 0.05) decrease in growth rate and an increased sensitivity to fresh porcine serum and high concentrations (more than 0.5 M) of sodium chloride. In DNA microarray experiments, the BALF-exposed  malT  mutant exhibited a gene-expression profile resembling that of a stringent type gene-expression profile seen in bacteria facing amino acid or carbon starvation. Genes encoding proteins for protein synthesis, energy metabolism, and DNA replication were down-regulated, while genes involved in stringent response (e.g.,  relA ), amino acid and nucleotide biosynthesis, biofilm formation, DNA transformation, and stress response were up-regulated.    Conclusion  These results suggest that MalT may be involved in protection against some stressors and in the transport of one or more essential nutrients in BALF. Moreover, if MalT is directly or indirectly linked to the stringent response, an important global mechanism of bacterial persistence and virulence in many bacterial pathogens, it might play a role in  A. pleuropneumoniae  pathogenesis.

malT knockout mutation invokes a stringent type gene-expression profile in Actinobacillus pleuropneumoniae in bronchoalveolar fluid