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Acute bronchitis is generally attributed to certain respiratory viruses, such as influenza virus A or B, respiratory syncytial virus, coronavirus, rhinoviruses, or others, although various bacteria have often been implicated in some cases, either as causative agents or as secondary agents following the initial virus infection (Gwaltney, 2002; Roxas & Jurenka, 2007; See & Wark, 2008). Chronic bronchitis may also be exacerbated by the same agents. These viruses and bacteria initially encounter epithelial tissues of the nose, oral mucosa, bronchi and airway linings, which are composed primarily of epithelial cells covered by a “soup” of proteins, glycoproteins, muco-polysaccharides, some of which possess intrinsic antimicrobial properties (Diamond et al., 2008; Evans et al., 2010). Interspersed among these epithelial cells are occasional phagocytes and various types of leukocyte. The epithelial and other cells possess a variety of pattern recognition receptors (PRRs), on and within the cells, which serve as molecular sensors. In response to the recognition of a pathogen various signaling pathways may be activated, resulting in the production and/or secretion of many pro-inflammatory cytokines and chemokines, as well as antimicrobial peptides and other inflammatory mediators. Further signaling among resident cells of the tissues, and migrating leukocytes attracted to the site of invasion, causes amplification of the output of inflammatory molecules. This situation may become chronic and lead to prolonged bronchitis. However, recent virological studies have shown that direct cytopathic damage by the pathogen is not a prerequisite for the induction of inflammatory mediators. For example, rhinoviruses and respiratory syncytial virus generally show limited replication and cause little or no cellular damage, yet they can induce large amounts of inflammatory cytokines (Mosser et al., 2005; Sharma et al., 2009a). Thus, the epithelium has a two-fold function in response to potential pathogens; it has a barrier function and also serves as a sensor that signals an efficient antimicrobial response. This is the primary component of the innate “immune” or “non-specific” host response (Diamond et al., 2008; Evans et al., 2010). However, incomplete elimination of the pathogen, or over-stimulation of the responses, can lead to an excessive or chronic inflammatory condition. Since the pathogens comprise such a heterogeneous collection of causative agents, this presents a formidable obstacle to the design of therapeutic strategies, which have in the past focused on curbing the growth of a specific virus or bacterium (Fedson, 2009; Ludwig, 2009).

Potential of the Phytomedicine Echinacea in the Treatment of Pulmonary Infections and Bronchitis