Table 3.

Immune responses towards acute Burkholderia pseudomallei infection: acute streptozotocin (STZ) -induced diabetes model versus acute normoglycaemic model

	Acute melioidosis infection (within 42-hr infection period)
Immune responses towards B. pseudomallei infection	STZ-diabetic model (this study)	Normoglycaemic model18
The TLR2 is responsible for recognition and initiation of defence response	TLR2 and several transcription factors were elevated 24hr p.i. in the diabetic liver	Rapid induction of TLR2. Several transcription factors were elevated as early as 16hr p.i. in both liver and spleen
Induction of various immune response genes, including the ‘core immune response’ genes to general inflammation infections	Most of the inflammatory genes were elevated only 24hr p.i. in the diabetic liver, but were mildly elevated after 42hr p.i. in the diabetic spleen	Rapid and overwhelmed inflammatory response throughout the infection period. Several potent chemokines were suppressed at 42hr p.i.
Activation of APPs lead to occurrence of tissue damage	Mild elevation of some APPs and proteasomal degradation-related genes after 24hr p.i. the liver	High induction of many APPs in the liver. Peptidoglysis and proteasomal degradation-related genes were elevated throughout the infection period in both liver and spleen
Activation of complement pathway	Not activated in response to infection	Complement pathway-related genes were mildly elevated after 24hr p.i. but some key genes of membrane attack complex formation were suppressed
Activation of various cell death mechanisms	Caspase and cell death-related genes were elevated in the liver 24hr p.i.	Caspase and inflammasome-related genes were elevated in both liver and spleen as early as 16hr p.i.

APP, acute-phase protein; p.i., post-infection; TLR, Toll-like receptor.