Abstract D.Z.is a 65-year-old man admitted to medical ward with an exacerbation of chronic obstructive pulmonary disease (COPD; emphysema). Past medical history (PMH) indicates hypertension (HTN), well managed with enalapril (Vasotec) past six years, diagnosis (Dx) of pneumonia yearly for the past three years. D.Z. appears cachectic with difficulty breathing at rest. Patient reports productive cough with thick yellow-green sputum. He seems anxious and irritable during subjective data collection. He states, he has been a 2-pack-a-day smoker for 38 years. He complains of (c/o) insomnia and While healthy lungs expand with each inhalation and collapse with each exhalation, helping to move air in and out of the lungs damaged by emphysema gradually lose their elasticity, becoming floppy and over-expanded like a spent rubber band. The airways normally held open by the elastic pull of the lungs, also become floppy and collapse on exhalation. As a result, patients with emphysema have increasing difficulty moving air in and out of their lungs. In relation to patients D.Z. with emphysema, the walls between the tiny air sacs in the lungs are damaged due to long-term cigarette smoking effect on his lungs as evidenced by his statements that, he finds it difficulty breathing even at rest (Rosdahl & Kowalski, 2003; Wedzicha & Seemungal, 2007). According to Peter J. Barnes of National Heart and Lung Institute, United Kingdom, the damage to lung function in patients with COPD and emphysema is related to a high percentage of CD4+ and CD8+ T lymphocytes that expressed chemokine receptors CCR5 and CXCR3 which are both indicators of T helper 1 cells, but not CCR3. Lung lymphocytes in patients with COPD and emphysema such as in the case of D.Z., secretes more interferon gamma, often associated with T helper 1 cells and interferon-inducible protein 10 and monokine induced by interferon, both of which bind to CXCR3 and are involved in drawing T helper 1 cells. In response to interferon-inducible protein 10 and monokine induced by
