Pasteurella multocida are Gram-negative coccobacilli causing various diseases in animals. Its pathogenesis is complex involving interaction between host and bacterial virulence factors. In this study we identified the role of cytokines and toll-like receptors in P. multocida infection. Three groups of BALB/c mice were setup. The first group received 2x102 CFU/ml P. multocida serotype B:2 (challenge group), the second group was vaccinated with formalin killed alum adjuvant P. multocida (vaccinated group) and the third control group received PBS. Equal numbers of animals from different groups were sacrificed to collect lung and liver tissues at various times of infection. Different cytokines IL-2, IL-4, IL-10, IFN-γ and TNF-α, and TLRs, TLR-1, -2, -4 and -6 were selected for regulatory effects of P. multocida infection in mice. The time-course of release showed statistically significant elevations of these cytokines in lung and liver tissues during early hours of infection. The relative fold change expression of cytokines and TLRs showed higher levels of IL-4 and IL-10 than IFN-γ, IL-2 and TNFα in challenge group when compared with vaccinated and control groups. The expression of TLR2 and TLR4 was also upregulated as compared to other TLRs. These results suggest the dominance of Th2 cytokines over Th1 cytokines in protective immunity against P. multocida infection. Additionally, the pathogen-associated virulence factors showed statistically significant upregulation of iron aquisition gene HgA and filamentous gene PfhA most prevalent in P. multocida serotype B as compared to less prevalent SodC. These virulence genes facilitated the colonization and invasion of host leading to the stimulation of host inflammatory response. Our findings suggest that P. multocida infection modulate inflammatory and immunological responses by altering the expression of its virulent genes.