**Author details**

causes of CAP are *S. pneumoniae, S. aureus*, and *H. influenzae. S. pneumoniae* is the most frequently isolated pathogen associated with influenza [60], although deaths, especially in children, are also associated with *S. aureus* infection, as highlighted by the recent emergence of community-acquired methicillin-resistant *S. aureus* [61]. Besides influenza, other respiratory viruses, such as coronavirus, adenovirus, and respiratory syncytial virus, are also associated

The mechanisms of superinfection are very complex process. Several reports indicate that changes due to virus in the respiratory tract prime the upper airway and lung make way for subsequent bacterial infection. Super bacterial infections are accompanied by virus-induced cytopathology, leading to immunological impairment, which could be caused in part by the overproduction of inflammatory cytokines [63]. Transformation of the immune response by curtailing the capacity of the host to clear bacteria may contribute to the severity of the resulting infection [64]. Earlier studies on animal model have demonstrated that influenza predisposes to bacterial pneumonia [63, 65, 66]. It has been reported with 7–21 days of lag time for the onset of bacterial infection following seasonal influenza. However, shorter times from

onset to death have been noticed in pandemic periods [67–69].

mucosal antibody responses and a cell-mediated response.

**8.5. Antibiotic adjuvants potentiate anti-inflammatory properties of antibiotics**

There is limited information on the effectiveness of adjuvant therapy for the treatment of bacterial complications of influenza. In a very recent study [70], explored the adjuvant effect of polyactin (PA), an inactivated trivalent influenza virus (ITIV) with or without PA or MF59 was instilled intranasally once a week in BALB/c mice. Results showed that PA is a novel mucosal adjuvant for intranasal vaccination with the inactivated trivalent influenza vaccine that has safe and effective mucosal adjuvanticity in mice and successfully induces both serum and

The inflammatory response of viral infections results in the excessive production of reactive oxygen species (ROS) in the cells and tissues, and antioxidant system cannot neutralize them. Imbalance in this protective mechanism can lead to the damage of cellular molecules such as DNA, proteins, and lipids [71]. Moreover, the role of ROS in inflammation has been investigated vigorously by earlier authors [72, 73]. ROS are thought to be key signaling molecules in the progression of inflammatory disorders. It induces inflammation by the induction of COX-2, inflammatory cytokines (TNFα, interleukin 1 (IL-1), and IL-6), chemokines (IL-8 and CXCR4), and pro-inflammatory transcription factors (NF-κB) [74]. Inflammatory cytokines trigger inflammation, causing the immune response to weaken which may help to increase the risk of bacterial infection. This rise in inflammatory markers with infection is a cascade reaction and is not easily broken only by antibiotics. Adjuvants have a major role to play here. Buret [75] reported that some antibiotics, such as the 16-membered macrolide tilmicosin, may generate anti-inflammatory benefits by modulating the production of pro-inflammatory mediators, and by inducing neutrophil apoptosis. Many studies have highlighted that adjuvants co-administered with antibiotics reduce the oxidative stress, which in turn reduce inflammation [76, 77]. Dwivedi et al. [78] reported that AAE used for 21 days, the levels of antioxidant enzymes (superoxidase dismutase, catalase, glutathione reductase, glutathione

with pneumonia [62].

134 Contemporary Topics of Pneumonia

Manu Chaudhary, Gazalla Ayub and Anurag Payasi\*

\*Address all correspondence to: ccmb@vmrcindia.com

Venus Medicine Research Centre, Hill Top Industrial Estate, Jharmajri EPIP, Bhatoli Kalan, India
