## 3 Results and Discussion
In our study, 9-methoxyellipticine could effectively lower the levels of TNF-\(\alpha\) and IgGM, and as a result it could effectively lower lung and kidney damage in _K. pneumoniae_ and STEC O157 infected mice, respectively. The positive control groups died prior to the end of the experiment. Analysis experimentation established that all mice were infested with great CFU loads, indicating that mortality rate was triggered by infection. An assessment of TNF-\(\alpha\) and IgM levels was performed to prove that _E. coli_ and _K. pneumoniae_ provoked proinflammatory conditions. However, treatment with 9-methoxyellipticine successfully led to normal levels of TNF-\(\alpha\) and IgM being exhibited (Figure 3A-D). In a previous survey, ellipticine notably reduced the levels of pro-inflammatory cytokines and chemokines, resulting in a dramatic reduction in the inflammatory cell infiltration [43]. These findings agreed with our study, as was revealed from biochemical markers and histopathological images and scoring. Furthermore, natural compounds that function as immunomodators are needed for improving the immune system, especially in infectious disorders. Ellipticine was reported to have a potent immunostimulant activity [44]. Our report documented the role of alkaloids in immunity, where 9-methoxyellipticine increased the levels of IgM to counter their reduced levels after the infection induced by _K. pneumoniae_ and STEC O157 in mice. _K. pneumoniae_ pulmonary lesions (Figure 4a-c) of the untreated positive control exhibited focal hemorrhages in the interstitial tissue and in the alveolar lamina in addition to dilated pulmonary blood vessels. Additionally, inflammatory infiltration composed of the histiocytes and polymorphonuclear sections was seen. In contrast, lungs infected with _K. pneumoniae_ subsequently treated by 9-methoxyellipticine revealed the moderate infiltration of inflammatory cells with the emphysema of pulmonary alveoli. Sections of _K. pneumoniae infection_ after treatment with GEN demonstrated an emphysema of pulmonary alveoli and a mild inflammatory cell infiltration in the lung tissue (Figure 4a-c). Treatment with 9-methoxyellipticine (Table 3) showed no indication of hemorrhage, no RBCs in alveolar lamina, and no perivascular oedema. More importantly, ellipticine was reported as a suggested treatment for the avoidance of acute death triggered by severe inflammation, with a noteworthy protective activity in _Streptococcus suis serotype 2_ strain-infected mice [45]. Figure 4: H&E of lungs of the mice infected by MDR _K. pneumoniae_. (**a**) Model group (\(\times\)400), (**b**) gentamycin(GEN)-treated group (\(\times\)200), and (**c**) 9-methoxyelliptic-treated group (\(\times\)400). Figure 3: Biochemical assessment of IgM (Immunoglobulin M) in mice infected by MDR _Klebsiella pneumoniae_ (**A**) and STEC O157 (Shiga-toxin-producing _Escherichia coli_) (**B**). Biochemical assessment of TNF-\(\alpha\) (Tumor necrosis factor alpha) in mice infected by MDR _Klebsiella pneumoniae_ (**C**) and STEC O157 (Shiga-toxin-producing _Escherichia coli_) (**D**). \({}^{\mathrm{a}}\) significant difference from the normal control group at \(p\) \(<\) 0.05. \({}^{\mathrm{b}}\) Significant difference from the infected group at \(p\) \(<\) 0.05. \({}^{\mathrm{ab}}\) Significant difference from both normal control and infected groups at \(p\) \(<\) 0.05. One day post _K. pneumoniae_ inoculation, the infected mice showed indications of quicker respiration, subordinate action, muddled bristle, or coat, and had intensified secretions around the infected eyes (Figure 5a-c and Table 4). Furthermore, these symptoms were faster after 48 h of immunization and the animal started to pass away; all animals died within 7 days in the positive control group, showing that _K. pneumoniae_ inoculation causes a critical pulmonary inflammatory response. However, in the 9-methoxyellipticine-treated group, the pulmonary hemorrhage and interalveolar thickness were significantly decreased.