For a fast and synthetic answer, it needs notions of General Pathology. There are biological events e.g. hypersensibility reactions and shock, that can help you to the comprehension of the phenomena.

The systemic inflammatory reactions could develop in situations of high risk of infection, generating a Systemic Inflammatory Response Syndrome (SIRS) and finally septic shock. Generally, the presence of lipid A of Lipo-polysaccharide (LPS) in the blood represents a trigger factor and the inflammatory cells produce TNFalfa, IL-1, predominantly. Briefly, it occurs generation of anaphylotoxins (fragments of complement system, C3a and C5a), Hageman Factor and kallikrein-kinin system activation, coagulation cascade activation, generation of inflammatory mediators e.g. prostaglandins, leukotrienes, thromboxane, PAF, cytokines, ROS, endothelial damage, etc.

Dear Antonella,

     Thanks for your answer. My point is simple in case of injury it will form the local inflammation so when and how this local inflammation will form systemic or spill over. Is there any particular pathways or mechanism that after a process local inflammation will become systemic??

From trauma/injury perspective, much work has been done to help elucidate this "spillover effect"; Specific aspects that warrant further consideration include:

1) Activation of common, distal pathways following the initiation of local (or proximal) inflammatory response. Some references here:

Goris, R. J. A. (1996). MODS/SIRS: result of an overwhelming inflammatory response?. World journal of surgery, 20(4), 418-421.

Lenz, A., Franklin, G. A., & Cheadle, W. G. (2007). Systemic inflammation after trauma. Injury, 38(12), 1336-1345.

2) The concept of "second hit" or "inflammatory priming" where someone exposed (either acutely or chonically) to inflammation may exhibit an exacerbated inflammatory response upon subsequent exposures:

Giannoudis, P. V. (2003). Current concepts of the inflammatory response after major trauma: an update. Injury, 34(6), 397-404.

http://www.jleukbio.org/content/78/4/819.short

Ogura, H., Tanaka, H., Koh, T., Hashiguchi, N., Kuwagata, Y., Hosotsubo, H., ... & Sugimoto, H. (1999). Priming, second-hit priming, and apoptosis in leukocytes from trauma patients. Journal of Trauma and Acute Care Surgery, 46(5), 774-783.

3) The concept of "immuno-senescence" or "inflamm-aging", based on the observations that low-grade "first hits" may result in exacerbated responses to "second hits" as it applies to ultra-long-term perspective and evolutionary pressures:

Franceschi, C., Bonafè, M., Valensin, S., Olivieri, F., de Luca, M., Ottaviani, E., & de Benedictis, G. (2000). Inflamm‐aging: an evolutionary perspective on immunosenescence. Annals of the New York Academy of Sciences, 908(1), 244-254.

Hope this helps; Upvote if helpful!

Cheers,

Stan.

Hello Stanislaw...Thank you for your kind answer. 

Dendritic and some other cells can carry the pathogen from the local cite of inflammation to the target organ that in turn might lead to systemic inflammation. This is the case for toxoplasma mediated encephalitis, salmonella infection, etc. It was shown that toxoplasma can actually increase the motility of dendritic cells and obviously effects their homing. Virulence systems (T3SS f.i.) of pathogens are of importance for this phenomenon.