CALCA and bacterial infectious disease: Interestingly, in case of severe bacterial infections, microbial products (e.g., LPS) and proinflammatory mediators of the host response (e.g., Tumor Necrosis Factor α and Interleukin-1β) result in a generalized tissuewide induction of calcitonin mRNA and a consequent secretion of calcitonin precursors including unprocessed PCT through a nonregulated constitutive pathway [3].